Medicine Surgery

Cardiac Structural Anomalies and Repair

Description

This cluster of papers focuses on surgical ventricular reconstruction and repair in the context of myocardial infarction, including topics such as postinfarction ventricular septal defect, ischemic and dilated cardiomyopathy, cardiac support devices, and coronary artery bypass. The papers discuss risk factors, outcomes, and various surgical techniques for addressing ventricular complications following myocardial infarction.

Keywords

Ventricular Reconstruction; Myocardial Infarction; Surgical Repair; Left Ventricular; Cardiac Support Device; Postinfarction Ventricular Septal Defect; Ischemic Cardiomyopathy; Dilated Cardiomyopathy; Cardiac Rupture; Coronary Artery Bypass

Abstract We present a case of a 34-year-old male with dilated cardiomyopathy in whom we performed a new surgical procedure; i.e., ventricular volume reduction to improve function. This initial human … Abstract We present a case of a 34-year-old male with dilated cardiomyopathy in whom we performed a new surgical procedure; i.e., ventricular volume reduction to improve function. This initial human experience was preceded by a series of ten sheep in which we demonstrated that by enlarging the left ventricle (LV), the ejection fraction was reduced, and by restoring normal diameter, the LV function returned to normal.
Whether culture-expanded mesenchymal stem cells or whole bone marrow mononuclear cells are safe and effective in chronic ischemic cardiomyopathy is controversial.To demonstrate the safety of transendocardial stem cell injection with … Whether culture-expanded mesenchymal stem cells or whole bone marrow mononuclear cells are safe and effective in chronic ischemic cardiomyopathy is controversial.To demonstrate the safety of transendocardial stem cell injection with autologous mesenchymal stem cells (MSCs) and bone marrow mononuclear cells (BMCs) in patients with ischemic cardiomyopathy.A phase 1 and 2 randomized, blinded, placebo-controlled study involving 65 patients with ischemic cardiomyopathy and left ventricular (LV) ejection fraction less than 50% (September 1, 2009-July 12, 2013). The study compared injection of MSCs (n=19) with placebo (n = 11) and BMCs (n = 19) with placebo (n = 10), with 1 year of follow-up.Injections in 10 LV sites with an infusion catheter.Treatment-emergent 30-day serious adverse event rate defined as a composite of death, myocardial infarction, stroke, hospitalization for worsening heart failure, perforation, tamponade, or sustained ventricular arrhythmias.No patient had a treatment-emergent serious adverse events at day 30. The 1-year incidence of serious adverse events was 31.6% (95% CI, 12.6% to 56.6%) for MSCs, 31.6% (95% CI, 12.6%-56.6%) for BMCs, and 38.1% (95% CI, 18.1%-61.6%) for placebo. Over 1 year, the Minnesota Living With Heart Failure score improved with MSCs (-6.3; 95% CI, -15.0 to 2.4; repeated measures of variance, P=.02) and with BMCs (-8.2; 95% CI, -17.4 to 0.97; P=.005) but not with placebo (0.4; 95% CI, -9.45 to 10.25; P=.38). The 6-minute walk distance increased with MSCs only (repeated measures model, P = .03). Infarct size as a percentage of LV mass was reduced by MSCs (-18.9%; 95% CI, -30.4 to -7.4; within-group, P = .004) but not by BMCs (-7.0%; 95% CI, -15.7% to 1.7%; within-group, P = .11) or placebo (-5.2%; 95% CI, -16.8% to 6.5%; within-group, P = .36). Regional myocardial function as peak Eulerian circumferential strain at the site of injection improved with MSCs (-4.9; 95% CI, -13.3 to 3.5; within-group repeated measures, P = .03) but not BMCs (-2.1; 95% CI, -5.5 to 1.3; P = .21) or placebo (-0.03; 95% CI, -1.9 to 1.9; P = .14). Left ventricular chamber volume and ejection fraction did not change.Transendocardial stem cell injection with MSCs or BMCs appeared to be safe for patients with chronic ischemic cardiomyopathy and LV dysfunction. Although the sample size and multiple comparisons preclude a definitive statement about safety and clinical effect, these results provide the basis for larger studies to provide definitive evidence about safety and to assess efficacy of this new therapeutic approach.clinicaltrials.gov Identifier: NCT00768066.
Since 1984, we have used a circular patch to reconstruct the left ventricle ("endoventricular circular plasty") in order to maintain a more physiologic cavity. This technique has three theoretical advantages … Since 1984, we have used a circular patch to reconstruct the left ventricle ("endoventricular circular plasty") in order to maintain a more physiologic cavity. This technique has three theoretical advantages over standard linear closure of the left ventricle (LV). First, it allows exclusion of the septal akinetic segment of the LV. Secondly, circular reorganization of the remaining LV muscle avoids the restraint caused by the linear suture closure and achieves a more physiologic LV cavity. Thirdly, circular plasty using the patch allows a complete resection of aneurysmal segments including resection of extensive subendocardial scar tissue, when appropriate, without critically compromising the cavity size.
Implantable left ventricular assist devices have benefited patients with end-stage heart failure as a bridge to cardiac transplantation, but their long-term use for the purpose of enhancing survival and the … Implantable left ventricular assist devices have benefited patients with end-stage heart failure as a bridge to cardiac transplantation, but their long-term use for the purpose of enhancing survival and the quality of life has not been evaluated.
Background— SCIPIO is a first-in-human, phase 1, randomized, open-label trial of autologous c-kit + cardiac stem cells (CSCs) in patients with heart failure of ischemic etiology undergoing coronary artery bypass … Background— SCIPIO is a first-in-human, phase 1, randomized, open-label trial of autologous c-kit + cardiac stem cells (CSCs) in patients with heart failure of ischemic etiology undergoing coronary artery bypass grafting (CABG). In the present study, we report the surgical aspects and interim cardiac magnetic resonance (CMR) results. Methods and Results— A total of 33 patients (20 CSC-treated and 13 control subjects) met final eligibility criteria and were enrolled in SCIPIO. CSCs were isolated from the right atrial appendage harvested and processed during surgery. Harvesting did not affect cardiopulmonary bypass, cross-clamp, or surgical times. In CSC-treated patients, CMR showed a marked increase in both LVEF (from 27.5±1.6% to 35.1±2.4% [ P =0.004, n=8] and 41.2±4.5% [ P =0.013, n=5] at 4 and 12 months after CSC infusion, respectively) and regional EF in the CSC-infused territory. Infarct size (late gadolinium enhancement) decreased after CSC infusion (by manual delineation: −6.9±1.5 g [−22.7%] at 4 months [ P =0.002, n=9] and −9.8±3.5 g [−30.2%] at 12 months [ P =0.039, n=6]). LV nonviable mass decreased even more (−11.9±2.5 g [−49.7%] at 4 months [ P =0.001] and −14.7±3.9 g [−58.6%] at 12 months [ P =0.013]), whereas LV viable mass increased (+11.6±5.1 g at 4 months after CSC infusion [ P =0.055] and +31.5±11.0 g at 12 months [ P =0.035]). Conclusions— Isolation of CSCs from cardiac tissue obtained in the operating room is feasible and does not alter practices during CABG surgery. CMR shows that CSC infusion produces a striking improvement in both global and regional LV function, a reduction in infarct size, and an increase in viable tissue that persist at least 1 year and are consistent with cardiac regeneration. Clinical Trial Registration— This study is registered with clinicaltrials.gov, trial number NCT00474461.
Background Although residual myocardial viability in patients with coronary artery disease and extensive regional asynergy is associated with improved ventricular function after coronary bypass surgery, the relationship between viability and … Background Although residual myocardial viability in patients with coronary artery disease and extensive regional asynergy is associated with improved ventricular function after coronary bypass surgery, the relationship between viability and clinical outcome after surgery is unclear. We hypothesized that patients with poor ventricular function and predominantly viable myocardium have a better outcome after bypass surgery compared with those with less viability. Methods and Results Seventy patients with multivessel coronary artery disease and left ventricular ejection fractions <40% who underwent preoperative quantitative 201 Tl scintigraphy before coronary bypass surgery were analyzed retrospectively. 201 Tl scintigrams were reviewed blindly, and each segment was assigned a score based on defect magnitude. Segmental viability scores were summed and divided by the number of segments visualized to determine a viability index. The viability index was significantly related to 3-year survival free of cardiac event (cardiac death or heart transplant) after bypass surgery ( P =.011) and was independent of age, ejection fraction, and number of diseased coronary vessels. Patients with greater viability (group 1; viability index >0.67; n=33) were similar to patients with less viability (group 2; viability index ≤0.67; n=37) with respect to age, comorbidities, and extent of coronary artery disease. There were 6 cardiac deaths and no heart transplants in group 1 patients and 15 cardiac deaths and two transplants in group 2 patients. Survival free of cardiac death or transplantation was significantly better in group 1 patients on Kaplan-Meier analysis ( P =.018). Conclusions We conclude that resting 201 Tl scintigraphy may be useful in preoperative risk stratification for identification of patients more likely to benefit from surgical revascularization.
OVER the past decade, percutaneous transluminal coronary angioplasty has gained wide acceptance as the procedure of choice in many patients with atherosclerotic coronary artery disease. As experience with the procedure … OVER the past decade, percutaneous transluminal coronary angioplasty has gained wide acceptance as the procedure of choice in many patients with atherosclerotic coronary artery disease. As experience with the procedure has grown, its rate of success has risen to approximately 90 percent and the incidence of acute complications has fallen; as a result, emergency coronary-artery bypass surgery is required in less than 4 percent of patients.1 2 3 Despite these improvements, re-Stenosis in the days, weeks, or months after successful angioplasty of a narrowed coronary artery occurs in 25 to 35 percent of patients,3 4 5 6 7 or 45 to 55 percent of those with . . .
A 74-year-old man with a history of hypertension and myocardial infarction that had occurred in the remote past presents with breathlessness on exertion. On examination, his pulse is 76 beats … A 74-year-old man with a history of hypertension and myocardial infarction that had occurred in the remote past presents with breathlessness on exertion. On examination, his pulse is 76 beats per minute and his blood pressure is 121/74 mm Hg. There is jugular venous distention and edema in the lower limbs; the lungs are clear. An echocardiogram shows left ventricular dilatation and an ejection fraction of 33%. How should his case be managed?
We prospectively recorded all in-hospital complications of the first 3500 consecutive patients to undergo elective coronary angioplasty (PTCA) at Emory University Hospitals from July 14, 1980, to August 28, 1984, … We prospectively recorded all in-hospital complications of the first 3500 consecutive patients to undergo elective coronary angioplasty (PTCA) at Emory University Hospitals from July 14, 1980, to August 28, 1984, by three operators. PTCA was attempted in a total of 3933 lesions, with a primary success rate of 91%. Multiple-lesion PTCA was performed in 401 patients, and PTCA of saphenous vein grafts was attempted in 172. No complications were recorded in 3116 (89%) cases, isolated minor complications occurred in 241 (6.9%), and major complications (emergency surgery, myocardial infarction, death) were observed in 145 (4.1%). Emergency coronary artery bypass graft surgery (CABG) was performed in 96 patients (2.7%), with a myocardial infarction rate of 49% (47/96), a Q wave infarction rate of 23% (22/96), and an emergency surgery mortality rate of 2% (2/96). Hospital discharge occurred within 2 weeks of attempted PTCA in 91% (87/96) of patients undergoing emergency CABG. The overall myocardial infarction rate was 2.6% (94/3500). There were two nonsurgical deaths, giving a total mortality rate of 0.1% (4/3500). Univariate and multivariate analysis of 3099 patients undergoing single-lesion PTCA identified five preprocedure predictors of a major complication: multivessel coronary disease, lesion eccentricity, presence of calcium in the lesion, female gender, and lesion length. Unstable angina, duration of angina, lesion severity, previous CABG, and vein graft dilatation were not associated with an increased incidence of major complications. The strongest predictor of a major complication was the procedural appearance of an intimal dissection. Intimal dissection was evident in 894/3099 (29%) patients.(ABSTRACT TRUNCATED AT 250 WORDS)
The leading cause of death in patients hospitalized for acute myocardial infarction is cardiogenic shock. We conducted a randomized trial to evaluate early revascularization in patients with cardiogenic shock. The leading cause of death in patients hospitalized for acute myocardial infarction is cardiogenic shock. We conducted a randomized trial to evaluate early revascularization in patients with cardiogenic shock.
The equatorial region of the canine left ventricle was modeled as a thick-walled cylinder consisting of an incompressible hyperelastic material with homogeneous exponential properties. The anisotropic properties of the passive … The equatorial region of the canine left ventricle was modeled as a thick-walled cylinder consisting of an incompressible hyperelastic material with homogeneous exponential properties. The anisotropic properties of the passive myocardium were assumed to be locally transversely isotropic with respect to a fiber axis whose orientation varied linearly across the wall. Simultaneous inflation, extension, and torsion were applied to the cylinder to produce epicardial strains that were measured previously in the potassium-arrested dog heart. Residual stress in the unloaded state was included by considering the stress-free configuration to be a warped cylindrical arc. In the special case of isotropic material properties, torsion and residual stress both significantly reduced the high circumferential stress peaks predicted at the endocardium by previous models. However, a resultant axial force and moment were necessary to cause the observed epicardial deformations. Therefore, the anisotropic material parameters were found that minimized these resultants and allowed the prescribed displacements to occur subject to the known ventricular pressure loads. The global minimum solution of this parameter optimization problem indicated that the stiffness of passive myocardium (defined for a 20 percent equibiaxial extension) would be 2.4 to 6.6 times greater in the fiber direction than in the transverse plane for a broad range of assumed fiber angle distributions and residual stresses. This agrees with the results of biaxial tissue testing. The predicted transmural distributions of fiber stress were relatively flat with slight peaks in the subepicardium, and the fiber strain profiles agreed closely with experimentally observed sarcomere length distributions. The results indicate that torsion, residual stress and material anisotropy associated with the fiber architecture all can act to reduce endocardial stress gradients in the passive left ventricle.
We quantified cardiovascular death and/or left ventricular (LV) dilatation in patients from the SAVE trial to determine whether dilatation continued beyond 1 year, whether ACE inhibitor therapy attenuated late LV … We quantified cardiovascular death and/or left ventricular (LV) dilatation in patients from the SAVE trial to determine whether dilatation continued beyond 1 year, whether ACE inhibitor therapy attenuated late LV dilatation, and whether any baseline descriptors predicted late dilatation.Two-dimensional echocardiograms were obtained in 512 patients at 11+/-3 days and 1 and 2 years postinfarction to assess LV size, percentage of the LV that was akinetic/dyskinetic (%AD), and LV shape index. LV function was assessed by radionuclide ejection fraction. Two hundred sixty-three patients (51.4%) sustained cardiovascular death and/or LV diastolic dilatation; 279 (54.5%) had cardiovascular death and/or systolic dilatation. In 373 patients with serial echocardiograms, LV end-diastolic and end-systolic sizes increased progressively from baseline to 2 years (both P<.01). More patients with LV dilatation had a decrease in ejection fraction: 24.8% versus 6.8% (P<.001) (diastole) and 25.7% versus 5.3% (P<.001) (systole). Captopril attenuated diastolic LV dilatation at 2 years (P=.048), but this effect was carried over from the first year of therapy because changes in LV size with captopril beyond 1 year were similar to those with placebo. Predictors of cardiovascular death and/or dilatation were age (P=.023), prior infarction (P<.001), lower ejection fraction (P<.001), angina (P=.007), heart failure (P=.002), LV size (P<.001), and infarct size (%AD) (P<.001).Cardiovascular death and/or LV dilatation occurred in >50% of patients by 2 years. LV dilatation is progressive, associated with chamber distortion and deteriorating function that is unaffected by captopril beyond 1 year.
BACKGROUND Ischemic cardiomyopathy is characterized by myocyte loss, reactive cellular hypertrophy, and ventricular scarring. However, the relative contribution of these tissue and cellular processes to late failure remains to be … BACKGROUND Ischemic cardiomyopathy is characterized by myocyte loss, reactive cellular hypertrophy, and ventricular scarring. However, the relative contribution of these tissue and cellular processes to late failure remains to be determined. METHODS AND RESULTS Ten hearts were obtained from individuals undergoing cardiac transplantation as a result of chronic coronary artery disease in its terminal stage. An identical number of control hearts were collected at autopsy from patients who died from causes other than cardiovascular disease, and morphometric methodologies were applied to the analysis of the left and right ventricular myocardium. Left ventricular hypertrophy evaluated as a change in organ weight, aggregate myocyte mass, and myocyte cell volume per nucleus showed increases of 85%, 47%, and 103%, respectively. Corresponding increases in the right ventricle were 75%, 74%, and 112%. Myocyte loss, which accounted for 28% and 30% in the left and right ventricles, was responsible for the difference in the assessment of myocyte hypertrophy at the ventricular, tissue, and cellular levels. Left ventricular muscle cell hypertrophy was accomplished through a 16% and 51% increase in myocyte diameter and length, whereas right ventricular myocyte hypertrophy was the consequence of a 13% and 67% increase in these linear dimensions, respectively. Moreover, a 36% reduction in the number of myocytes included in the thickness of the left ventricular wall was found. Collagen accumulation in the form of segmental, replacement, and interstitial fibrosis comprised an average 28% and 13% of the left and right ventricular myocardia, respectively. The combination of cell loss and myocardial fibrosis, myocyte lengthening, and mural slippage of cells resulted in 4.6-fold expansion of left ventricular cavitary volume and a 56% reduction in the ventricular mass-to-chamber volume ratio. CONCLUSIONS These results are consistent with the contention that both myocyte and collagen compartments participate in the development of decompensated eccentric ventricular hypertrophy in the cardiomyopathic heart of ischemic origin.
In a double-blind trial of streptokinase for acute myocardial infarction, 219 consecutive patients presenting with infarction within four hours (mean, 3.0±0.8) of the onset of chest pain were randomly assigned … In a double-blind trial of streptokinase for acute myocardial infarction, 219 consecutive patients presenting with infarction within four hours (mean, 3.0±0.8) of the onset of chest pain were randomly assigned to treatment with streptokinase (1.5 million units) or placebo, given intravenously over 30 minutes. The primary end point of the study was left ventricular function in patients with first infarctions. Patients who could undergo beta-blockade also received intravenous propranolol. Heparin (for 48 hours) and a combination of low-dose aspirin and dipyridamole were administered to both groups until cineangiography was performed at three weeks. In the patients with first infarctions treated with streptokinase, the left ventricular ejection fraction was 6 percentage points higher (streptokinase vs. placebo, 59±10.5 vs. 53±13.5 percent; P<0.005), with benefit to patients with either anterior infarction (57±11.9 vs. 49±15.9 percent; P<0.05) or inferior infarction (60±9.1 vs. 55±11.3 percent; P<0.05). Left ventricular function was improved regardless of whether concomitant propranolol was given. Survival (at 30 days) was improved with streptokinase: 2 deaths occurred among 79 patients who received this drug, as compared with 12 deaths among 93 patients who received placebo (2.5 vs. 12.9 percent, P = 0.012). Rates of reinfarction (streptokinase vs. placebo, 3 vs. 1 percent) and requirements for surgery or angioplasty (7 vs. 5 percent) were similar in the two groups. We conclude that administration of intravenous streptokinase (1.5 million units) to patients with a first myocardial infarction results in improved left ventricular function and short-term survival. (N Engl J Med 1987; 317: 850–5.)
Recent studies demonstrated that the "no reflow" phenomenon after coronary reflow implies the presence of advanced myocardial damage. In this study, we verified the prognostic value of the detection of … Recent studies demonstrated that the "no reflow" phenomenon after coronary reflow implies the presence of advanced myocardial damage. In this study, we verified the prognostic value of the detection of this phenomenon by studying complications, left ventricular morphology, and in-hospital survival after acute myocardial infarction (AMI).The study population consisted of 126 patients with a first anterior AMI. All patients received coronary reflow within 24 hours of onset of symptoms and underwent myocardial contrast echocardiography (MCE) before and shortly after coronary reflow with an intracoronary injection of sonicated microbubbles. From contrast reperfusion patterns, patients were divided into two subsets: those with MCE no reflow (47 patients, 37%) and those with MCE reflow (79 patients). There was no difference in the frequency of arrhythmia or coronary events between the two subsets. Pericardial effusion and early congestive heart failure were observed more frequently in patients with MCE no reflow than in those with MCE reflow (26% versus 4%, P < .05; 45% versus 15%, P < .05, respectively). Congestive heart failure tended to be prolonged in those with MCE no reflow, and 3 patients (7%) of this subset died of pump failure. Left ventricular end-diastolic volume progressively increased in the convalescent stage in patients with MCE no reflow (early versus late, 145 +/- 43 versus 169 +/- 60 mL, P < .001), whereas it decreased in those with MCE reflow (154 +/- 42 versus 144 +/- 44 mL, P < .01).The substantial size of the MCE no reflow phenomenon at coronary reflow conveys useful information about an outcome of coronary intervention and left ventricular remodeling in individual patients with anterior wall AMI, although these are suggestive results in a limited number of patients.
The CardioWest Total Artificial Heart orthotopically replaces both native cardiac ventricles and all cardiac valves, thus eliminating problems commonly seen in the bridge to transplantation with left ventricular and biventricular … The CardioWest Total Artificial Heart orthotopically replaces both native cardiac ventricles and all cardiac valves, thus eliminating problems commonly seen in the bridge to transplantation with left ventricular and biventricular assist devices, such as right heart failure, valvular regurgitation, cardiac arrhythmias, ventricular clots, intraventricular communications, and low blood flows.We conducted a nonrandomized, prospective study in five centers with the use of historical controls. The purpose was to assess the safety and efficacy of the CardioWest Total Artificial Heart in transplant-eligible patients at risk for imminent death from irreversible biventricular cardiac failure. The primary end points included the rates of survival to heart transplantation and of survival after transplantation.Eighty-one patients received the artificial-heart device. The rate of survival to transplantation was 79 percent (95 percent confidence interval, 68 to 87 percent). Of the 35 control patients who met the same entry criteria but did not receive the artificial heart, 46 percent survived to transplantation (P<0.001). Overall, the one-year survival rate among the patients who received the artificial heart was 70 percent, as compared with 31 percent among the controls (P<0.001). One-year and five-year survival rates after transplantation among patients who had received a total artificial heart as a bridge to transplantation were 86 and 64 percent.Implantation of the total artificial heart improved the rate of survival to cardiac transplantation and survival after transplantation. This device prevents death in critically ill patients who have irreversible biventricular failure and are candidates for cardiac transplantation.
Background 99m Tc sestamibi is a recently developed radioisotope that has been used to measure myocardium at risk and infarct size. The relation between these measurements and subsequent patient outcome … Background 99m Tc sestamibi is a recently developed radioisotope that has been used to measure myocardium at risk and infarct size. The relation between these measurements and subsequent patient outcome has not yet been demonstrated. Methods and Results Two hundred seventy-four consecutive patients with acute myocardial infarction underwent tomographic 99m Tc sestamibi imaging on arrival at the hospital (to measure myocardium at risk before reperfusion therapy) and at hospital discharge (to measure the amount of salvaged myocardium and final infarct size). Defect size on the sestamibi images was quantified using a threshold value of 60% of peak counts from the circumferential count profile curves generated for five representative slices of the left ventricle. Patients were followed after hospital discharge to evaluate the association between final infarct size and subsequent mortality. The median defect size measured was 27% of the left ventricle at presentation to the hospital (range, 0% to 77%) and was 12% of the left ventricle at hospital discharge (range, 0% to 68%). Almost one half of the patients had a final infarct size of ≤10%. The median amount of myocardium salvaged was 9% (range, −31% to 75%). During a median duration of follow-up of 12 months, there were 10 deaths (7 cardiac and 3 noncardiac) and 1 resuscitated out-of-hospital cardiac arrest. There was a significant association between infarct size and overall mortality (χ 2 =8.66, P =.003) and cardiac mortality (χ 2 =11.89, P &lt;.001). Two-year mortality was 7% for patients whose infarct size was ≥12% versus 0% for patients whose infarct size was &lt;12%. There also was a significant association between myocardium at risk and cardiac mortality (χ 2 =6.87, P =.009). There was no association between myocardium at risk and overall mortality or between amount of myocardium salvaged and either overall mortality or cardiac mortality. Conclusions Larger infarct size measured by 99m Tc sestamibi imaging after acute myocardial infarction is associated with increased mortality risk during short-term follow-up.
Background —Ventricular septal defect (VSD) complicating acute myocardial infarction has been studied primarily in small, prethrombolytic-era trials. Our goal was to determine clinical predictors and angiographic and clinical outcomes of … Background —Ventricular septal defect (VSD) complicating acute myocardial infarction has been studied primarily in small, prethrombolytic-era trials. Our goal was to determine clinical predictors and angiographic and clinical outcomes of this complication in the thrombolytic era. Methods and Results —We compared enrollment characteristics, angiographic patterns, and outcomes (30-day and 1-year mortality) of patients enrolled in the Global Utilization of Streptokinase and TPA for Occluded Coronary Arteries (GUSTO-I) trial with and without a confirmed diagnosis of VSD. Univariable and multivariable analyses were used to assess relations between enrollment factors and the development of VSD. In all, 84 of the 41 021 patients (0.2%) developed VSD, a smaller percentage than reported in the prethrombolytic era. The median time from symptom onset to VSD diagnosis was 1 day. Enrollment factors most associated with this complication were advanced age, anterior infarction, female sex, and no previous smoking. The infarct artery was more often the left anterior descending and more likely to be totally occluded in patients who developed VSD. Mortality at 30 days was higher in patients with VSDs than in those without this complication (73.8% versus 6.8%, P &lt;0.001). Patients with VSDs selected for surgical repair (n=34) had better outcomes than patients treated medically (n=35; 30-day mortality, 47% versus 94%). Conclusions —Compared with historical control subjects, patients who undergo thrombolysis within 6 hours of infarction onset may have a reduced risk of later VSD. If patients develop this mechanical complication, however, it typically occurs sooner than described in the prethrombolytic era. Despite improvements in medical therapy and percutaneous and surgical techniques, mortality with this complication remains extremely high.
ARDIOGENIC SHOCK (CS) IS the leading cause of death for patients hospitalized with acute myocardial infarction (AMI), 1,2 and mortality remains high during the following year. 3,4The SHOCK (Should We … ARDIOGENIC SHOCK (CS) IS the leading cause of death for patients hospitalized with acute myocardial infarction (AMI), 1,2 and mortality remains high during the following year. 3,4The SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) Trial demonstrated a nonsignificant reduction in 30day mortality (56% vs 47%) when early revascularization (ERV) was compared with a strategy of initial medical stabilization (IMS), with a larger difference between the groups at 6 months. 5In this article, we report the 1-year survival, a prespecified secondary end point of the SHOCK Trial.
Background: Survival is poor in patients with acute myocardial infarction (MI) who also have severe renal disease. Less is known about the outcome of acute MI in patients with mild … Background: Survival is poor in patients with acute myocardial infarction (MI) who also have severe renal disease. Less is known about the outcome of acute MI in patients with mild to moderate renal insufficiency. Objective: To compare outcomes after acute MI in patients with varying levels of renal disease and in patients without renal failure. Design: Retrospective cohort study. Setting: Academic medical center. Patients: 3106 total patients admitted with acute MI and end-stage renal disease (n = 44), severe renal insufficiency (creatinine clearance < 0.59 mL/s [<35 mL/min]) (n = 391), moderate renal dysfunction (creatinine clearance ≥ 0.59 mL/s [<35 mL/min] but ≤ 0.84 mL/s [≤ 50 mL/min]) (n = 491), mild chronic renal insufficiency (creatinine clearance > 0.84 mL/s [>50 mL/min] but ≤ 1.25 mL/s [≤ 75 mL/min]) (n = 860), or no renal disease (n = 1320). Measurements: Clinical characteristics, treatment strategies, and short- and long-term survival were compared after patients were stratified by creatinine clearance. Results: In-hospital mortality rates were 2% in patients with normal renal function, 6% in those with mild renal failure, 14% in those with moderate renal failure, 21% in those with severe renal failure, and 30% in those with end-stage renal disease (P < 0.001). Compared with patients without renal disease, similar adjusted trends were present for postdischarge death in patients with end-stage renal disease (hazard ratio, 5.4 [95% CI, 3.0 to 9.7]; P < 0.001), severe renal insufficiency (hazard ratio, 1.9 [CI, 1.2 to 3.0]; P = 0.006), moderate renal dysfunction (hazard ratio, 2.2 [CI, 1.5 to 3.3]; P < 0.001), and mild chronic renal insufficiency (hazard ratio, 2.4 [CI, 1.7 to 3.3]; P < 0.001). Patients with renal failure received adjunctive and reperfusion therapies less frequently than those with normal renal function (P < 0.001). Postdischarge death was less likely in patients who received acute reperfusion therapy (odds ratio, 0.7 [CI, 0.6 to 0.9]), aspirin (odds ratio, 0.7 [CI, 0.5 to 0.8]), and β-blocker therapy (odds ratio, 0.7 [CI, 0.6 to 0.9]). Conclusion: Patients with renal failure are at increased risk for death after acute MI and receive less aggressive treatment than patients with normal renal function.
Surgical ventricular reconstruction is a specific procedure designed to reduce left ventricular volume in patients with heart failure caused by coronary artery disease. We conducted a trial to address the … Surgical ventricular reconstruction is a specific procedure designed to reduce left ventricular volume in patients with heart failure caused by coronary artery disease. We conducted a trial to address the question of whether surgical ventricular reconstruction added to coronary-artery bypass grafting (CABG) would decrease the rate of death or hospitalization for cardiac causes, as compared with CABG alone.Between September 2002 and January 2006, a total of 1000 patients with an ejection fraction of 35% or less, coronary artery disease that was amenable to CABG, and dominant anterior left ventricular dysfunction that was amenable to surgical ventricular reconstruction were randomly assigned to undergo either CABG alone (499 patients) or CABG with surgical ventricular reconstruction (501 patients). The primary outcome was a composite of death from any cause and hospitalization for cardiac causes. The median follow-up was 48 months.Surgical ventricular reconstruction reduced the end-systolic volume index by 19%, as compared with a reduction of 6% with CABG alone. Cardiac symptoms and exercise tolerance improved from baseline to a similar degree in the two study groups. However, no significant difference was observed in the primary outcome, which occurred in 292 patients (59%) who were assigned to undergo CABG alone and in 289 patients (58%) who were assigned to undergo CABG with surgical ventricular reconstruction (hazard ratio for the combined approach, 0.99; 95% confidence interval, 0.84 to 1.17; P=0.90).Adding surgical ventricular reconstruction to CABG reduced the left ventricular volume, as compared with CABG alone. However, this anatomical change was not associated with a greater improvement in symptoms or exercise tolerance or with a reduction in the rate of death or hospitalization for cardiac causes. (ClinicalTrials.gov number, NCT00023595.)
Cardiogenic shock remains the major cause of death for patients hospitalized with acute myocardial infarction (MI). Although survival in patients with cardiogenic shock complicating acute MI has been shown to … Cardiogenic shock remains the major cause of death for patients hospitalized with acute myocardial infarction (MI). Although survival in patients with cardiogenic shock complicating acute MI has been shown to be significantly higher at 1 year in those receiving early revascularization vs initial medical stabilization, data demonstrating long-term survival are lacking.To determine if early revascularization affects long-term survival of patients with cardiogenic shock complicating acute MI.The Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock (SHOCK) trial, an international randomized clinical trial enrolling 302 patients from April 1993 through November 1998 with acute myocardial infarction complicated by cardiogenic shock (mean [SD] age at randomization, 66 [11] years); long-term follow-up of vital status, conducted annually until 2005, ranged from 1 to 11 years (median for survivors, 6 years).All-cause mortality during long-term follow-up.The group difference in survival of 13 absolute percentage points at 1 year favoring those assigned to early revascularization remained stable at 3 and 6 years (13.1% and 13.2%, respectively; hazard ratio [HR], 0.74; 95% confidence interval [CI], 0.57-0.97; log-rank P = .03). At 6 years, overall survival rates were 32.8% and 19.6% in the early revascularization and initial medical stabilization groups, respectively. Among the 143 hospital survivors, a group difference in survival also was observed (HR, 0.59; 95% CI, 0.36-0.95; P = .03). The 6-year survival rates for the hospital survivors were 62.4% vs 44.4% for the early revascularization and initial medical stabilization groups, respectively, with annualized death rates of 8.3% vs 14.3% and, for the 1-year survivors, 8.0% vs 10.7%. There was no significant interaction between any subgroup and treatment effect.In this randomized trial, almost two thirds of hospital survivors with cardiogenic shock who were treated with early revascularization were alive 6 years later. A strategy of early revascularization resulted in a 13.2% absolute and a 67% relative improvement in 6-year survival compared with initial medical stabilization. Early revascularization should be used for patients with acute MI complicated by cardiogenic shock due to left ventricular failure.clinicaltrials.gov Identifier: NCT00000552.
When Is Enough Enough?Bodh I. Jugdutt, MD L eft ventricular (LV) remodeling after myocardial in- farction (MI) contributes significantly to LV dilation and dysfunction, and disability and death.Two paradigms, pertinent … When Is Enough Enough?Bodh I. Jugdutt, MD L eft ventricular (LV) remodeling after myocardial in- farction (MI) contributes significantly to LV dilation and dysfunction, and disability and death.Two paradigms, pertinent to antiremodeling therapy after MI (Figure 1), have evolved over the last 3 decades.Paradigm 1, LV remodeling is a major mechanism for disability and death, 1,2 has received a great deal of attention.In contrast, paradigm 2, remodeling of the extracellular collagen matrix (ECCM) plays a major role in LV remodeling, [3][4][5][6][7] whereby decrease, disruption, and/or defective composition of the ECCM promote LV dilation and rupture, 4 -7 has received little attention.A host of clinical trials showed that angiotensin-converting enzyme (ACE) inhibitors (ACE-Is) with or without aldosterone antagonists, angiotensin II (AngII) type 1 (AT 1 ) receptor blockers (ARBs), ␤-adrenergic blockers or reperfusion improve outcome in survivors of MI. 8 -10 Concurrent evidence has underscored the importance of preserving the ECCM during healing after MI. 2-7 However, the antifibrotic action of ACE-Is, aldosterone antagonists and ARBs on ECCM in the infarct zone (IZ) and noninfarct zone (NIZ), 6,7,9,11 and the reperfusion-induced damage to the ECCM in the IZ, 5,7,12 remain unreconciled with the benefits. 8 -10,13 Nevertheless, excessive ECCM, as in dilated ischemic cardiomyopathy after remote MI, 14,15 can contribute to LV diastolic dysfunction and poor outcome, 6 suggesting that antifibrotic drugs that target excess ECCM might be a logical therapeutic approach.This review focuses on the role of the ECCM in the evolution of LV remodeling after MI and the potential impact of therapies that target the ECCM. Ventricular Remodeling After MI and the Role of ECCMFive points merit emphasis.First, the LV remodeling process after MI is complex, dynamic, and time dependent, and progresses in parallel with healing over months. 1,2,7,16Notably, it involves differential changes between the IZ and NIZ with respect to the following: (1) LV structure, shape, and topography 1,2 (Figure 1); (2) cell type, such as myocytes and nonmyocytes (Table 1) 6,7,[17][18][19][20][21][22][23] ; (3) proteins, cytokines, and growth factors 7,24,25 ; and (4) the ECCM. 5-7,13-17,19 -23 Differential re-gional remodeling of the ECCM contributes significantly to global LV structural remodeling after MI (Figure 2) 7,9,26 and plays a pivotal role in paradigm 1. 3,6,7 Second, the post-MI heart shows remarkable capacity to adapt to the rather sudden development of an IZ and a NIZ.Thus, MI results in time-dependent damage to myocytes, nonmyocytes, and the ECCM in the IZ; ventricular dysfunction followed by volume overload and progressive dilation; reactive hypertrophy with interstitial fibrosis and increased collagen in the NIZ; gradual reparative fibrosis in the IZ 27 ; and vascular remodeling in the IZ and NIZ. 7hird, several endogenous molecules that affect collagen synthesis and are upregulated after MI, and several agents that are used therapeutically for MI, affect collagen turnover (Table 2, Figure 3) and exert an antifibrotic effect. 2,7,9,10,28his can potentially alter ECCM remodeling in the IZ 9,28 and impair healing, 29 and thereby promote adverse remodeling and outcome, depending on their timing relative to pathophysiological stages of healing (Table 3).Fourth, a fine balance, between matrix metalloproteinases (MMPs) that degrade ECCM and endogenous tissue inhibitors of MMPs (TIMPs) that inhibit MMPs, 30 -32 maintains normal remodeling and function, and an imbalance can result in adverse remodeling. 24,25,30,33,34ifth, although a 2-to 3-fold increase in myocardial collagen above the normal level results in increased LV stiffness and mild dysfunction, 35 a very small decrease in collagen below normal can lead to drastic consequences, 36,37 including LV dilation 4,22,34 and rupture. 33,38In reperfused MI, decreased or damaged ECCM in the IZ 5,12,39 is associated with cardiac rupture. 5,39
Background Ventricular dilation, indexed by marked shifts toward larger volumes of the end-diastolic pressure-volume relation (EDPVR), has been considered to represent an irreversible aspect of ventricular remodeling in end-stage heart … Background Ventricular dilation, indexed by marked shifts toward larger volumes of the end-diastolic pressure-volume relation (EDPVR), has been considered to represent an irreversible aspect of ventricular remodeling in end-stage heart failure. However, we hypothesized that such dilation could be reversed with sufficient hemodynamic unloading, such as can be provided by a left ventricular assist device (LVAD). Methods and Results The EDPVRs of hearts from seven patients with end-stage idiopathic cardiomyopathy and comparable baseline hemodynamics were measured ex vivo at the time of cardiac transplantation; these were compared with EDPVRs from three normal human hearts that were technically unsuitable for transplantation. Four of the patients received optimal medical therapy; three of the patients, who deteriorated on optimal therapy, underwent LVAD support for ≈4 months. Compared with the normal hearts, EDPVRs of hearts from medically treated patients were shifted toward markedly larger volumes. In contrast, EDPVRs of hearts from LVAD patients were similar to those of normal hearts. Conclusions Chronic hemodynamic unloading of sufficient magnitude and duration can result in reversal of chamber enlargement and normalization of cardiac structure as indexed by the EDPVR, both important aspects of remodeling, even in the most advanced stages of heart failure.
Phase I clinical studies have demonstrated the feasibility of implanting autologous skeletal myoblasts in postinfarction scars. However, they have failed to determine whether this procedure was functionally effective and arrhythmogenic.This … Phase I clinical studies have demonstrated the feasibility of implanting autologous skeletal myoblasts in postinfarction scars. However, they have failed to determine whether this procedure was functionally effective and arrhythmogenic.This multicenter, randomized, placebo-controlled, double-blind study included patients with left ventricular (LV) dysfunction (ejection fraction < or = 35%), myocardial infarction, and indication for coronary surgery. Each patient received either cells grown from a skeletal muscle biopsy or a placebo solution injected in and around the scar. All patients received an implantable cardioverter-defibrillator. The primary efficacy end points were the 6-month changes in global and regional LV function assessed by echocardiography. The safety end points comprised a composite index of major cardiac adverse events and ventricular arrhythmias. Ninety-seven patients received myoblasts (400 or 800 million; n=33 and n=34, respectively) or the placebo (n=30). Myoblast transfer did not improve regional or global LV function beyond that seen in control patients. The absolute change in ejection fraction (median [interquartile range]) between 6 months and baseline was 4.4% (0.2; 7.3), 3.4% (-0.3; 12.4), and 5.2% (-4.4; 11.0) in the placebo, low-dose, and high-dose groups, respectively (P=0.95). However, the high-dose cell group demonstrated a significant decrease in LV volumes compared with the placebo group. Despite a higher number of arrhythmic events in the myoblast-treated patients, the 6-month rates of major cardiac adverse events and of ventricular arrhythmias did not differ significantly between the pooled treatment and placebo groups.Myoblast injections combined with coronary surgery in patients with depressed LV function failed to improve echocardiographic heart function. The increased number of early postoperative arrhythmic events after myoblast transplantation, as well as the capability of high-dose injections to revert LV remodeling, warrants further investigation.
Cardiac remodeling is defined as a group of molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart after injury. The … Cardiac remodeling is defined as a group of molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart after injury. The process results in poor prognosis because of its association with ventricular dysfunction and malignant arrhythmias. Here, we discuss the concepts and clinical implications of cardiac remodeling, and the pathophysiological role of different factors, including cell death, energy metabolism, oxidative stress, inflammation, collagen, contractile proteins, calcium transport, geometry and neurohormonal activation. Finally, the article describes the pharmacological treatment of cardiac remodeling, which can be divided into three different stages of strategies: consolidated, promising and potential strategies.
The survival benefit of a strategy of coronary-artery bypass grafting (CABG) added to guideline-directed medical therapy, as compared with medical therapy alone, in patients with coronary artery disease, heart failure, … The survival benefit of a strategy of coronary-artery bypass grafting (CABG) added to guideline-directed medical therapy, as compared with medical therapy alone, in patients with coronary artery disease, heart failure, and severe left ventricular systolic dysfunction remains unclear.
We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients … We conducted a double-blind, placebo-controlled trial to determine whether ventricular dilatation continues during the late convalescent phase after myocardial infarction and whether therapy with captopril alters this process. Fifty-nine patients with a first anterior myocardial infarction and a radionuclide ejection fraction of 45 percent or less underwent cardiac catheterization 11 to 31 days after infarction, when they were not in overt congestive heart failure. They were randomly assigned to placebo or captopril and were followed for one year. A repeat catheterization was performed to evaluate interval changes in hemodynamic function and left ventricular volume. Thirty-eight male patients were evaluated with maximal-exercise treadmill tests every three months. No differences were detected at base line in clinical, hemodynamic, or quantitative ventriculographic variables. During one year of follow-up, the end-diastolic volume of the left ventricle increased by a mean [±SEM] of 21 ±8 ml (P<0.02) in the placebo group, but by only 10±6 ml (P not significant) in the captopril group. The left ventricular filling pressure remained elevated with placebo but decreased (P<0.01) with captopril. In a subset of 36 patients who were at high risk for ventricular enlargement because they had persistent occlusion of the left anterior descending coronary artery, captopril prevented further ventricular dilatation (P<0.05). Patients given captopril also had increased exercise capacity (P<0.05). This preliminary study indicates that after anterior myocardial infarction, ventricular enlargement is progressive and that captopril may attenuate this process, reduce filling pressures, and improve exercise tolerance. (N Engl J Med 1988; 319:80–6.)
Objective: To evaluate the outcome of single vs. bilateral internal thoracic artery (SITA vs. BITA) revascularization in patients with multivessel coronary disease referred for coronary artery bypass graft (CABG) while … Objective: To evaluate the outcome of single vs. bilateral internal thoracic artery (SITA vs. BITA) revascularization in patients with multivessel coronary disease referred for coronary artery bypass graft (CABG) while on chronic dialysis. Methods: This retrospective analysis included all the patients with multivessel disease on chronic dialysis who underwent isolated CABG in our center during 1996–2021, utilizing SITA or BITA revascularization. We further matched the groups according to patient age and EuroSCORE II ±0.5. Results: Of the 7547 patients with multivessel disease who underwent CABG, 77 were on chronic dialysis. Of these, 2 had incomplete follow-up data, 58 underwent SITA, and 17 BITA revascularization. Comparing the SITA group with the BITA, the mean age was higher (67.8 vs. 58.6 years, standardized mean difference 1.035); the median (interquartile range) EuroSCORE II was higher (3.73 (1.78–6.23) vs. 1.78 (1.38–3.50), standardized mean difference 0.934); and comorbidities were more prevalent. Early mortality did not differ between the BITA and SITA groups in the unmatched cohort (11.8% vs. 15.5%, p &gt; 0.999) or in the matched cohort (12.5% vs. 6.3%, p = 0.999). Other early adverse events such as early stroke, myocardial infarction, and bleeding requiring re-exploration were also similar. The median survival was 1.22 ± 0.5 years for the SITA and 5.64 ± 1.50 years for the BITA group. The respective five-year survival rates were 22.5 ± 5.9% and 58.35 ± 13.80%, p = 0.005. For the matched cohort, comprising 16 patient pairs, the five-year survival did not differ between the groups (27.8 ± 11.7% vs. 54.7 ± 14.7%, p = 0.258). In multivariable analysis, adjusted to EuroSCORE II and age, the hazard ratio (95% confidence interval) for BITA revascularization was insignificant, 0.638 (95% CI 0.25–1.62), p = 0.343. The hazard ratios for age and EuroSCORE II were 1.061 (95% CI 1.023–1.101), p = 0.002 and 1.155 (95% CI 1.070–1.246), p &lt; 0.001. Conclusions: Despite a trend in favor of BITA utilization, no clear long-term survival benefit was demonstrated for BITA revascularization in patients on chronic dialysis after CABG.
Introduction: The implantation of a left ventricular assist device (LVAD) is a life-saving therapeutic option for patients with advanced heart failure. The treatment goal has to be determined prior to … Introduction: The implantation of a left ventricular assist device (LVAD) is a life-saving therapeutic option for patients with advanced heart failure. The treatment goal has to be determined prior to LVAD implantation. However, prognostic evaluation for defining the treatment goal could be improved for a time- and cost-effective medical treatment. Methods: Our study comprised seven patients who were weaned from LVAD (recovery group) and a control group without weaning (non-recovery group; n = 7). Myocardial tissue was analysed for connective tissue content by Masson–Goldner trichrome staining and for collagen I and collagen III expression by quantitative real-time PCR and immunohistochemistry. Results: The histological evaluation revealed comparable values for the percentage of total connective tissue (non-recovery: 46.3% [95% CI: 15.9–76.7], recovery: 43.4% [95% CI: 13.7–73.2], p = 0.43). mRNA expression analysis for collagen I and III expression could not detect a difference in collagen I (p = 0.16) and collagen III expression (p = 0.12) between the non-recovery and the recovery group. Immunohistochemical staining revealed that the percentages of collagen I (p = 0.05) and of collagen III (p = 0.01) were reduced in patients who do not recover compared to patients who recover under LVAD support. Conclusions: Our data indicate that histological evaluation for collagen expression prior to LVAD implantation could detect differences in the collagen content that could be helpful for estimating the weaning success.
Background and Clinical Significance: Perforation of the left ventricle related to microaxial ventricular assist devices (Impella) is a rare but fatal complication related to placement or adjustment. It results in … Background and Clinical Significance: Perforation of the left ventricle related to microaxial ventricular assist devices (Impella) is a rare but fatal complication related to placement or adjustment. It results in left ventricular hemorrhage and tamponade, leading to rapid deterioration and death. Case Presentation: We present a case report of a 73-year-old man who developed this complication postoperatively and was successfully managed to a full recovery. Conclusions: To our knowledge, he is the only reported patient to have this complication outside the setting of immediate placement who subsequently survived to discharge.
Introduction Free wall rupture is a rare complication of myocardial infarction, occurring as early as a few hours after myocardial infarction. It usually happens after transmural myocardial infarction and has … Introduction Free wall rupture is a rare complication of myocardial infarction, occurring as early as a few hours after myocardial infarction. It usually happens after transmural myocardial infarction and has a very high mortality rate. The diagnosis of free wall rupture requires echocardiographic evidence of pericardial leakage or pericardial tamponade. The patient's cause of death is often attributed to other causes such as cardiac arrhythmia unless determined by open heart surgery or autopsy. Diagnostic tools for post-infarction cardiac free wall rupture are limited to date. Case presentation We present a case of myocardial infarction in a patient who presented with atypical chest pain. Subsequent coronary angiography revealed small vessel disease, however, the patient's severe clinical presentation was not consistent with small vessel disease. The initial clinical presentation did not rule out aortic dissection, prompting further investigation through aortic computed tomography. This imaging technique revealed a rupture of the free wall of the heart accompanied by a large amount of bloody pericardial effusion. Unfortunately, attempts to puncture and drain the effusion were unsuccessful and the patient eventually succumbed. Conclusions When patients present with more severe clinical manifestations that are not consistent with myocardial infarction, it is important to be alert to the possibility of cardiac rupture in addition to identifying the possibility of aortic dissection. Aortic CTA may be able to confirm the diagnosis of cardiac rupture.
Introducción: El aumento de la resistencia vascular pulmonar, evaluada por cateterismo derecho suele citarse como una contraindicación relativa para la inclusión en lista de trasplante cardíaco, debido a que se … Introducción: El aumento de la resistencia vascular pulmonar, evaluada por cateterismo derecho suele citarse como una contraindicación relativa para la inclusión en lista de trasplante cardíaco, debido a que se asocia a la falla del ventrículo derecho implantado. Existe evidencia que sugiere que el comportamiento de la circulación pulmonar depende de su interacción con el ventrículo derecho por lo que un parámetro que evalúe el acople ventrículo-arterial podría predecir la falla del ventrículo derecho mejor que parámetros hemodinámicos aislados. Objetivos: El objetivo de este estudio fue evaluar la capacidad de la relación TAPSE/PSP de predecir la incidencia de falla del ventrículo derecho postrasplante en relación con parámetros hemodinámicos invasivos medidos antes del trasplante. Material y Métodos: Estudio de cohorte retrospectiva en el que se utilizan variables recolectadas en forma prospectiva de la base de trasplante cardíaco de un Hospital Universitario de la Ciudad de Buenos Aires. Se incluyeron 56 pacientes consecutivos sometidos a trasplante cardíaco entre enero de 2012 y abril de 2017, de los cuales se contaba con la totalidad de las variables ecocardiográficas y hemodinámicas. Se excluyeron los pacientes con trasplante de más de un parénquima, los retrasplantes, aquellos con cardiopatías congénitas, los que presentaron requerimiento de asistencia ventricular al momento de la evaluación pretrasplante y los pacientes con datos incompletos. Resultados: Tres pacientes (5,3%) fallecieron dentro de los primeros 30 días, en 2 de estos se objetivó falla del ventrículo derecho. Ningún parámetro hemodinámico ni ecocardiográfico preoperatorio se asoció con mortalidad. La incidencia de falla del ventrículo derecho en el posoperatorio inmediato fue del 28,5% (16 pacientes). Todas las variables hemodinámicas de presión y resistencia pulmonar, y la relación TAPSE/PSP medida por ecocardiografía se asociaron con el desarrollo de falla del ventrículo derecho postrasplante. Luego de realizar un análisis multivariado que incluyó variables hemodinámicas y ecocardiográficas, la relación TAPSE/PSP fue la única que se asoció en forma independiente con falla del ventrículo derecho(OR &gt; 10; IC95 2,2-&gt; 100; p = 0,03). Un valor de corte de TAPSE/PSP de 0,26 mostró una sensibilidad de 81% y una especificidad de 88% para predecir la falla del ventrículo derecho, con un ABC ROC de 0,84 ± 0,06 y el valor de X2 en la prueba de Hosmer-Lemeshow fue 0 (p = 1) al considerar cuartiles de TAPSE/PSP. Un modelo predictivo de falla de ventrículo derecho compuesto por variables hemodinámicas mostró una sensibilidad del 38% y una especificidad del 97,5%, con un área bajo la curva ROC de 0,78 ± 0,06 y un valor de X2 en la prueba de Hosmer Lemeshow de 2,37 (p = 0,3). Conclusiones: Podemos concluir que la relación TAPSE/PSP mostró una mejor discriminación y calibración para predecir la falla del ventrículo derecho, y 0,26 fue el valor con mejor desempeño pronóstico.
A 4-day-old, 3.7-kg neonate presented to our institution with a systolic heart murmur and signs of respiratory distress and was found to have a giant left atrial appendage aneurysm on … A 4-day-old, 3.7-kg neonate presented to our institution with a systolic heart murmur and signs of respiratory distress and was found to have a giant left atrial appendage aneurysm on transthoracic echocardiogram. Given the compression of the left ventricle and signs of respiratory failure necessitating mechanical ventilation, the decision was made to proceed with surgical resection under cardiac arrest with cardiopulmonary bypass.
Ayman El‐Menyar | European Journal of Trauma and Emergency Surgery
A ventricular septal defect (VSD) is a rare but critical complication of acute myocardial infarction (AMI), occurring in up to 0.2% of patients undergoing a percutaneous coronary intervention (PCI). An … A ventricular septal defect (VSD) is a rare but critical complication of acute myocardial infarction (AMI), occurring in up to 0.2% of patients undergoing a percutaneous coronary intervention (PCI). An inferior VSD is less common than anterior VSD but has a worse prognosis, often presenting with hypotension, dyspnea, and a new holosystolic murmur. Two patient cases are provided of post-AMI VSD, following right coronary artery (RCA) infarction, both initially treated with PCI. In both these patient cases, echocardiography identified a basal inferoseptal aneurysm, with an 8.0-mm defect and a shunt. Both patients were referred for surgical intervention based on these diagnostic findings. This low-level evidence highlights the variability and severity of post-AMI VSD, in these patients. Despite advancements in reperfusion therapy, vigilant monitoring for late complications and timely intervention can be crucial and may improve outcomes, for this life-threatening condition.
Qiao Yang , Song Xue , Chao Ren +6 more | European Journal of Nuclear Medicine and Molecular Imaging
A comprehensive understanding of the genome-wide regulatory landscape of the cardiac tissues post-myocardial infarction (MI) is still lacking. We therefore integrated single-cell RNA sequencing (scRNA-seq) and single-cell for transposase-accessible chromatin … A comprehensive understanding of the genome-wide regulatory landscape of the cardiac tissues post-myocardial infarction (MI) is still lacking. We therefore integrated single-cell RNA sequencing (scRNA-seq) and single-cell for transposase-accessible chromatin sequencing (scATAC-seq) to elucidate the epigenetic landscape of the heart post-MI. We established MI mice through ligation of the left anterior descending coronary artery, and obtained cardiac tissues from mice at 1,3,7 and 14-day post-MI. Integrative analyses of the scRNA-seq and scATAC-seq data revealed the presence of two novel fibroblast subpopulations in the MI cardiac tissues, termed GATA-binding protein 5/ISL LIM Homeobox 1 (GATA5/ISL1) + fibroblasts and GLI family zinc finger 3 (Gli3) high fibroblasts. The GATA5/ISL1+ fibroblasts were characterized by fibroblast and cardiomyocyte signatures and were found to play a crucial role in cardiac repair post-MI. Moreover, adenoviral-mediated overexpression of GATA5 and ISL1 ameliorated cardiac function and attenuated myocardial fibrosis in the MI mice. RNA sequencing confirmed that GATA5 and ISL1 co-regulate Wnt signaling pathway to promote the transformation of fibroblasts into functional cardiomyocytes. Furthermore, analysis of the human cardiac tissues of MI patients also revealed the presence of GATA5/ISL1+ fibroblasts in the scar tissues, suggesting their crucial role in cardiac tissue repair post-MI. In addition, proteomic analyses revealed enhanced cardiac repair and development signaling in the GATA5/ISL1-overexpressing human cardiac fibroblasts. The study provides novel perspectives on the mechanisms of myocardial injury and repair at the single-cell level and indicates the potential role of GATA5 and ISL1 as therapeutic targets for MI treatment.
A. Leandro Barros , Daniel García‐Arribas , Javier Morán +3 more | Medicine - Programa de Formación Médica Continuada Acreditado