Bone marrow transplantation modulates tissue macrophage phenotype and enhances cardiac recovery after subsequent acute myocardial infarction.

BACKGROUND: Bone marrow transplantation (BMT) is commonly used in experimental studies to investigate the contribution of BM-derived circulating cells to different disease processes. During studies investigating the cardiac response to acute myocardial infarction (MI) induced by permanent coronary ligation in mice that had previously undergone BMT, we found that BMT itself affects the remodelling response. METHODS AND RESULTS: Compared to matched naive mice, animals that had previously undergone BMT developed significantly less post-MI adverse remodelling, infarct thinning and contractile dysfunction as assessed by serial magnetic resonance imaging. Cardiac rupture in male mice was prevented. Histological analysis showed that the infarcts of mice that had undergone BMT had a significantly higher number of inflammatory cells, surviving cardiomyocytes and neovessels than control mice, as well as evidence of significant haemosiderin deposition. Flow cytometric and histological analyses demonstrated a higher number of alternatively activated (M2) macrophages in myocardium of the BMT group compared to control animals even before MI, and this increased further in the infarcts of the BMT mice after MI. CONCLUSIONS: The process of BMT itself substantially alters tissue macrophage phenotype and the subsequent response to acute MI. An increase in alternatively activated macrophages in this setting appears to enhance cardiac recovery after MI.

Haploinsufficiency of Hand1 improves mice survival after acute myocardial infarction through preventing cardiac rupture.

Previous studies have demonstrated a significantly lower level of Hand1 in ischemic cardiomyopathy than in normal heart tissue. The role of decreased Hand1 in myocardial infarction remains unclear. This study was designed to investigate the effects of haploinsufficiency of Hand1 on mouse heart after myocardial infarction. 8-10 weeks old male heterozygous Hand1-deficient (Hand1(+/-)) mice and wild-type littermates (control) were subjected to sham operation or ligation of the left anterior descending coronary artery to induce acute myocardial infarction (AMI). Hand1(+/-) mice have low incidence of left ventricular free wall rupture in the first week after operation than control mice. Then we found lower MMP9 activity and less cardiomyocytes apoptosis in Hand1(+/-) than in control mice. All of these contribute to the protection role of haploinsufficiency of Hand1 after AMI.

Lack of phospholipase A2 receptor increases susceptibility to cardiac rupture after myocardial infarction.

RATIONALE: Recent evidence indicates that the biological effects of secretory phospholipase A2 (sPLA2) cannot be fully explained by its catalytic activity. A cell surface receptor for sPLA2 (PLA2 receptor 1 [PLA2R]) and its high-affinity ligands (including sPLA2-IB, sPLA2-IIE, and sPLA2-X) are expressed in the infarcted myocardium. OBJECTIVE: This study asked whether PLA2R might play a pathogenic role in myocardial infarction (MI) using mice lacking PLA2R (PLA2R(-/-)). METHODS AND RESULTS: MI was induced by permanent ligation of the left coronary artery. PLA2R(-/-) mice exhibited higher rates of cardiac rupture after MI compared with PLA2R wild-type (PLA2R(+/+)) mice (46% versus 21%, respectively; P=0.015). PLA2R(-/-) mice had a 31% decrease in collagen content and a 45% decrease in the number of α-smooth muscle actin-positive fibroblasts in the infarcted region compared with PLA2R(+/+) mice. PLA2R was primarily found in myofibroblasts in the infarcted region. PLA2R(-/-) myofibroblasts were impaired in collagen-dependent migration, proliferation, and activation of focal adhesion kinase in response to sPLA2-IB. Binding of sPLA2-IB to PLA2R promoted migration and proliferation of myofibroblasts through functional interaction with integrin ß1, independent of the catalytic activity of sPLA2-IB. In rescue experiments, the injection of PLA2R(+/+) myofibroblasts into the infarcted myocardium prevented post-MI cardiac rupture and reversed the decrease in collagen content in the infarcted region in PLA2R(-/-) mice. CONCLUSIONS: PLA2R deficiency increased the susceptibility to post-MI cardiac rupture through impaired healing of the infarcted region. This might be partly explained by a reduction in integrin ß1-mediated migratory and proliferative responses of PLA2R(-/-) myofibroblasts.

Cardiac Rupture: New Features of the Old Disease.

OBJECTIVES: Myocardial rupture is a rare but a fatal complication of acute myocardial infarction. During recent years, treatment strategies of acute myocardial infarction have changed. Primary percutaneous coronary interventions have replaced fibrinolytic therapy, thus reducing one of the major risk factors for myocardial rupture. In this work, we describe a group of patients who suffered myocardial rupture, none of whom were treated with thrombolytic therapy. METHODS: The digital database of our hospital was searched for all patients who experienced myocardial rupture between 2008 and 2015. The demographic, clinical, angiographic and echocardiographic data of these patients were analyzed. RESULTS: Out of 2,380 patients admitted with acute myocardial infarction, 12 (0.5%) developed myocardial rupture. The mean age was 78 years, and there were 7 males and 5 females. Ten patients already had pericardial effusion on admission. Seven patients underwent coronary angiography, whilst primary percutaneous intervention was performed in 4 patients. Six patients entered the operating room and all survived the procedure. All patients who were treated conservatively died due to rupture. Factors related to the treatment strategy were advanced age (≥ 90 years) and cognitive impairment. CONCLUSIONS: The risk of myocardial rupture may be diminished by primary coronary intervention during myocardial infarction, but mortality remains high. An early, comprehensive echocardiographic examination and rapid surgery may contribute to improved survival.

Glycogen synthase kinase-3α limits ischemic injury, cardiac rupture, post-myocardial infarction remodeling and death.

BACKGROUND: The molecular pathways that regulate the extent of ischemic injury and post-myocardial infarction (MI) remodeling are not well understood. We recently demonstrated that glycogen synthase kinase-3α (GSK-3α) is critical to the heart's response to pressure overload. However, the role, if any, of GSK-3α in regulating ischemic injury and its consequences is not known. METHODS AND RESULTS: MI was induced in wild-type (WT) versus GSK-3α((-/-)) (KO) littermates by left anterior descending coronary artery ligation. Pre-MI, WT, and KO hearts had comparable chamber dimensions and ventricular function, but as early as 1 week post-MI, KO mice had significantly more left ventricular dilatation and dysfunction than WT mice. KO mice also had increased mortality during the first 10 days post-MI (43% versus 22%; P=0.04), and postmortem examination confirmed cardiac rupture as the cause of most of the deaths. In the mice that survived the first 10 days, left ventricular dilatation and dysfunction remained worse in the KO mice throughout the study (8 weeks). Hypertrophy, fibrosis, and heart failure were all increased in the KO mice. Given the early deaths due to rupture and the significant reduction in left ventricular function evident as early as 1 week post-MI, we examined infarct size following a 48-hour coronary artery ligation and found it to be increased in the KO mice. This was accompanied by increased apoptosis in the border zone of the MI. This increased susceptibility to ischemic injury-induced apoptosis was also seen in cardiomyocytes isolated from the KO mice that were exposed to hypoxia. Finally, Bax translocation to the mitochondria and cytochrome C release into the cytosol were increased in the KO mice. CONCLUSION: GSK-3α confers resistance to ischemic injury, at least in part, via limiting apoptosis. Loss of GSK-3α promotes ischemic injury, increases risk of cardiac rupture, accentuates post-MI remodeling and left ventricular dysfunction, and increases the progression to heart failure. These findings are in striking contrast to multiple previous reports in which deletion or inhibition of GSK-3ß is protective.

Factors related to heart rupture in acute coronary syndromes in the Global Registry of Acute Coronary Events.

AIMS: To determine the incidence and factors associated with heart rupture (HR) in acute coronary syndrome (ACS) patients. METHODS AND RESULTS: Among 60 198 patients, 273 (0.45%) had HR (free wall rupture, n = 118; ventricular septal rupture, n = 155). Incidence was 0.9% for ST-segment elevation myocardial infarction (STEMI), 0.17% for non-STEMI, and 0.25% for unstable angina. Hospital mortality was 58 vs. 4.5% in patients without HR (P < 0.001). The incidence was lower in STEMI patients with primary percutaneous coronary intervention (PCI) than in those without (0.7 vs. 1.1%; P = 0.01), but primary PCI was not independently related to HR in adjusted analysis (P = 0.20). Independent variables associated with HR included: ST-segment elevation (STE)/left bundle branch block; ST-segment deviation; female sex; previous stroke; positive initial cardiac biomarkers; older age; higher heart rate; systolic blood pressure/30 mmHg decrease. Conversely, previous MI and the use of low-molecular-weight heparin and beta-blockers during first 24 h were identified as protective factors for HR. CONCLUSION: The incidence of HR is low in patients with ACS, although its incidence is probably underestimated. Heart rupture occurs more frequently in ACS with STE and is associated with high hospital mortality. A number of variables are independently related to HR.

Mitral Valve Surgery for Papillary Muscle Rupture: Outcomes in 1342 Patients From The Society of Thoracic Surgeons Database.

BACKGROUND: Prior reports of mitral valve surgery (MVS) for ischemic papillary muscle rupture (PMR) have been limited in patient numbers. This study evaluated national outcomes of MVS for PMR using The Society of Thoracic Surgeons (STS) National Database. METHODS: The study cohort was composed of patients undergoing MVS for ischemic PMR between 2011 and 2018 in the STS registry. Concomitant procedures were included. The primary outcome was operative mortality. Secondary outcomes included STS major morbidities. Multivariable logistic regression was employed for risk adjustment using clinically important variables as well as those predictive in univariate analysis. RESULTS: A total of 1342 patients underwent MVS for PMR during the study period. Most of these were mitral valve replacements (79.8%; n = 1071) and were performed emergently (52.0%; n = 698). Concomitant coronary artery bypass grafting was performed in 59.3% (n = 796). Mechanical circulatory assistance before MVS included intraaortic balloon pump (56.9%; n = 764), Impella pump (4.1%; n = 55), and extracorporeal membrane oxygenation (3.1%; n = 41). The STS predicted risk for mortality was 16.9% ± 15.4%. Operative mortality was 20.0%. Blood products were transfused in 70.7% (n = 949). Major morbidity rates included prolonged ventilation (61.8%; n = 829), acute renal failure (15.4%; n = 206), reoperation (10.2%; n = 137), and stroke (5.2%; n = 70). Multivariable predictors of operative mortality included mitral valve replacement, older age, lower albumin, cardiogenic shock, ejection fraction less than 25%, and emergent salvage status. CONCLUSIONS: These data provide a national overview of outcomes after MVS for PMR. Rates of mortality and morbidity are high, but most patients survive operative intervention in this high-risk and otherwise lethal condition.

Outcomes of emergency or urgent mitral valve repair in patients with papillary muscle rupture and active infective endocarditis.

BACKGROUND: Emergency or urgent surgery is often required in patients with papillary muscle rupture and active mitral valve infective endocarditis. The aim of this study was to analyze the outcomes of patients with active endocarditis who underwent emergency or urgent mitral valve repair. METHODS: From 2005 to 2014, 154 ischemic mitral regurgitation patients and 41 infective endocarditis patients underwent mitral valve repair in our institution; 23 had emergency operations due to papillary muscle rupture, and 18 with active infective endocarditis underwent urgent surgery. RESULTS: Cardiopulmonary bypass time (141.4 ± 43.3 versus 145.3 ± 46.5 min) and crossclamp time (77.7 ± 34.1 versus 79.2 ± 33.0 min) were similar in the papillary muscle rupture and elective ischemic mitral regurgitation subgroups, and major postoperative complications were comparable. Hospital mortality was 17.4% in the papillary muscle rupture subgroup and 8.4% in the elective ischemic mitral regurgitation subgroup. Cardiopulmonary bypass time (103.6 ± 37.0 versus 75.5 ± 20.8 min) and crossclamp time (61.7 ± 21.2 versus 45.3 ± 18.0 min) were significantly longer in infective endocarditis patients. There were no major complications or hospital deaths. Eight years postoperatively, overall survival was 94.4% and 86.5% in the papillary muscle rupture and elective ischemic mitral regurgitation subgroups, respectively (p = 0.730). Overall survival was 100% in both infective endocarditis subgroups. CONCLUSION: The feasibility and effectiveness of emergency or urgent mitral valve repair in patients with papillary muscle rupture and active infective endocarditis are satisfactory. Early and mid-term outcomes are comparable to those of elective operations.

Changes in hospital mortality rates in 425 patients with acute ST-elevation myocardial infarction and cardiac rupture over a 30-year period.

BACKGROUND: Possible changes in the incidence and outcome of cardiac rupture in patients with ST-elevation myocardial infarction over a long period of time have not been investigated. METHODS AND RESULTS: The incidence of cardiac rupture in ST-elevation myocardial infarction patients and its mortality rate were investigated during a 30-year period divided into 5 intervals (1977 to 1982, 1983 to 1988, 1989 to 1994, 1995 to 2000, and 2001 to 2006). Of a total of 6678 consecutive patients, 425 experienced a free wall rupture (280 with cardiac tamponade: 227 with electromechanical dissociation and 53 with hypotension) or a septal rupture (145). After the exclusion of referrals from other centers (n=44), the incidence of definite cardiac rupture (septal rupture, anatomic evidence of free wall rupture, or electromechanical dissociation) declined progressively (6.2% in 1977 to 1982 to 3.2% in 2001 to 2006; P<0.001) in parallel with a progressive use of reperfusion therapy (0% to 75.1%; P<0.001). In addition, among patients with cardiac rupture, there was a progressive fall in the rate of death (94% to 75%; P<0.001) despite a trend toward increasing age (66+/-8 to 75+/-8 years; P<0.054) in conjunction with better control of systolic blood pressure at 24 hours (130+/-24 versus 110+/-18 mm Hg; P<0.001); an increased use of reperfusion therapy (0% to 59%; P<0.001), beta-blockers (0% to 45%; P<0.001), angiotensin-converting enzyme inhibitors (0% to 38%; P<0.001), and aspirin (0% to 96%; P<0.001); and a lower use of heparin (99% to 67%; P<0.001). CONCLUSIONS: The decline in the incidence in cardiac rupture and its rate of death over the last 30 years appears to be associated with the increasing use of reperfusion strategies and adjunct medical therapy.

Blunt cardiac rupture: a 5-year NTDB analysis.

OBJECTIVE: Because of its rarity and high rate of mortality, traumatic blunt cardiac rupture (BCR) has been poorly studied. The objective of this study was to use the National Trauma Data Bank to review the epidemiology and outcomes associated with traumatic BCR. METHODS: After approved by the institutional review board, the National Trauma Data Bank (version 5.0) was queried for all BCR occurring between 2000 and 2005. Demographics, clinical injury data, interventions, and outcomes were abstracted for each patient. Statistical analysis was performed using an unpaired Student's t test or Mann-Whitney U test to compare means and chi analysis to compare proportions. Stepwise logistic regression analysis was performed to identify independent predictors of inhospital mortality. RESULTS: Of 811,531 blunt trauma patients, 366 (0.045%) had a BCR of which 334 were available for analysis, with the mean age of 45 years, 65% were men, and their mean Injury Severity Score was 58 +/- 19. The most common mechanism of injury was motor vehicle collision (73%), followed by pedestrian struck by auto (16%), and falls from height (8%). Twenty-one patients (6%) died on arrival and 140 (42%) died in the emergency room. The overall mortality for patients arriving alive to hospital was 89%. Of the patients surviving to operation, 42% survived >24 hours of which 87% were discharged. Survivors were significantly younger (39 vs. 46 years, p = 0.04), had a lower Injury Severity Score (47 vs. 56, p = 0.02), higher Glasgow Coma Scale (10 vs. 6, p < 0.001), and were more likely to present with an systolic blood pressure >or=90 mm Hg (p = 0.01). Nevertheless, none of these factors was found to be an independent risk factor for mortality. CONCLUSION: BCR is an exceedingly rare injury, occurring in 1 of 2400 blunt trauma patients. In patients arriving alive to hospital, traumatic BCR is associated with a high mortality rate, however, is not uniformly fatal.

Causes and temporal trends in procedural deaths after transcatheter aortic valve implantation.

BACKGROUND: The causes of procedural deaths after transcatheter aortic valve implantation (TAVI) have been scarcely detailed. AIMS: To assess these causes and their temporal trends since the beginning of the TAVI era. METHODS: From October 2006 to April 2014, 601 consecutive high-risk/inoperable patients with severe aortic stenosis underwent TAVI using the Edwards SAPIEN or SAPIEN XT or the Medtronic CoreValve. The transfemoral route was the default approach; the transapical or left subclavian approaches were alternative options. Patients were divided into three tertiles according to the date of the procedure. RESULTS: Procedural death occurred in 45 patients (7.5%), with a median±standard deviation age of 83±7 years; 23 were men (51%) and the mean logistic EuroSCORE was 26±16%. The main cause of death was heart failure (n=19, 42%), followed by cardiac rupture (n=12, 27%), intensive care complications (n=9, 20%) and vascular complications (n=5, 11%). The mortality rate was higher after transapical than transfemoral TAVI (17% vs. 5%; P<0.001). The mortality rate decreased over time (11.9% in the first tertile, 6.0% in the second and 4.5% in the third [P=0.007]), driven by a reduction in heart failure-related deaths (6.5% in the first tertile vs. 1.5% in the third; P=0.011). Vascular complication-related deaths disappeared in the third tertile. However, there was no decrease in deaths related to cardiac ruptures and intensive care complications. CONCLUSIONS: The procedural mortality rate of TAVI decreased over time, driven by the decrease in heart failure-related deaths. However, efforts should continue to prevent cardiac ruptures and improve the outcomes of patients requiring intensive care after TAVI.

Prognostic implications of PR-segment depression in inferior leads in acute inferior myocardial infarction.

BACKGROUND: Concurrent atrial ischemia is usually overlooked in acute myocardial infarction (MI) due to its subtle electrocardiographic (ECG) changes, lack of clear-cut clinical picture, and prognostic significance. PR-segment depression in the inferior leads is a simplified ECG sign for detecting possible underlying atrial ischemia. HYPOTHESIS: The purpose of this study was to document the incidence, clinical characteristics, and prognostic implications of this ECG sign in the setting of acute inferior MI. METHODS: Demographics, clinical characteristics, and outcomes of 463 consecutive patients presenting with acute inferior MI were reviewed. The in-hospital ECG was examined by two independent reviewers. The results were then compared between those with and without ECG sign. RESULTS: Profound PR-segment depression > or = 1.2 mm in inferior leads was found in 9 of 463 (1.9%) patients. Patients with atrial ischemia tended to present earlier (2.4 +/- 2.6 vs. 7.0 +/- 8.2 h, p = 0.000) and had a higher frequency of first-degree atrioventricular block (77.8 vs. 30.6%, p = 0.028) and supraventricular arrhythmias (55.5 vs. 20.2%, p = 0.022). Of greater importance, it was significantly associated with an increased rate of cardiac free-wall rupture (33.3 vs. 2.0%, p = 0.001) and in-hospital mortality (44.4 vs. 11.7%, p = 0.015). CONCLUSION: Profound PR-segment depression > or = 1.2 mm in inferior leads was associated with a complicated hospital course and poor short-term outcome in acute inferior MI. These patients were at high risk for the development of atrioventricular block, supraventricular arrhythmias, and cardiac free-wall rupture.

Outcome of primary percutaneous coronary intervention in octogenarians with acute myocardial infarction.

BACKGROUND/PURPOSE: Acute myocardial infarction (AMI) results in more complications and increased mortality in octogenarians compared to patients in younger age groups. This study investigated the short- and long-term outcomes in octogenarians after primary percutaneous coronary intervention (PCI). METHODS: During the study period from May 1997 to August 2004, 54 patients > or = 80 years old with ST-elevation myocardial infarction (STEMI) were eligible for primary PCI. Data collected included baseline clinical characteristics and usage of cardiovascular medications. Diagnostic coronary angiography and revascularization procedures were performed using standard practices. During hospitalization, the clinical course including serial changes in cardiac enzymes, adverse events associated with myocardial infarction or treatment, and inhospital or long-term mortality of patients were recorded. RESULTS: The mean age of the 54 patients (35 men, 19 women) was 82.8 +/- 2.5 years (range, 80-89 years). Among them, 27 (50%) had anterior infarction, six (11%) had anterolateral infarction, and 21 (39%) had inferior infarction, inclusive of three patients with accompanying right ventricular infarction. Among them, 20 (37%) patients were in Killip class I, nine (17%) were in class II, two (4%) in class III, and 23 (43%) in class IV. The mean delay from onset of symptoms to arrival in hospital was 220 +/- 167 minutes, and 189 +/- 169 minutes from hospital arrival to reperfusion. Diagnostic coronary angiography revealed that 48 (89%) patients had multivessel disease. Inhospital death occurred in 23 (43%) patients, with the leading causes of death being profound cardiogenic shock (61%), and free wall rupture (26%). CONCLUSION: Octogenarian patients who developed STEMI tended to have multivessel disease. These patients had a high inhospital mortality rate that was most likely to be due to cardiogenic shock.

Mitral valve replacement early after myocardial infarction: attendant high risk of left ventricular rupture.

Between 1969 and 1983, 608 patients underwent mitral valve replacement surgery at Cedars-Sinai Medical Center. Perioperative rupture of the left ventricular myocardium complicated seven operations (1.2%), five of them in the 247 patients with concomitant ischemic heart disease. Six ruptures were fatal. Relative incidences of seven previously hypothesized predisposing factors were determined for patients with and without myocardial rupture. In addition, because of the apparent frequency of association with ischemic heart disease and because all ruptures were posterior or posterolateral, patients were also categorized by prior history of posterior myocardial infarction: 177 patients had none, whereas 49 patients had a remote and 21 patients a recent (less than or equal to 1 month) posterior wall infarct. Four ruptures (accounting for 57% of all ruptures) occurred in the 21 patients (19% incidence) with a recent posterior infarct, compared with only three ruptures in the 587 patients (0.5%) without a recent posterior wall infarct (p = 0.000). None of the factors of age, sex, valve pathology, etiology of valve lesion, concomitant coronary disease, valve substitute or intraoperative myocardial preservation were associated with perioperative rupture. These data establish a low overall incidence of ventricular rupture after mitral valve replacement, high fatality and possible etiologic association with recent posterior wall infarction.

Cardiac rupture, mortality and the timing of thrombolytic therapy: a meta-analysis.

This study examined the relation between the risk of cardiac rupture and the timing of thrombolytic therapy for acute myocardial infarction. To test the hypothesis that cardiac rupture is prevented by early thrombolytic therapy but is promoted by late treatment, randomized controlled trials of thrombolytic agents for myocardial infarction were pooled. A logistic regression model including 58 cases of cardiac rupture among 1,638 patients from four trials showed that the odds ratio (treated/control) of cardiac rupture was directly correlated with time to treatment (p = 0.01); at 7 h, the odds ratio was 0.4 (95% confidence limits 0.17 to 0.93); at 11 h, it was 0.93 (0.53 to 1.60) and at 17 h, it was 3.21 (1.10 to 10.1). Analysis of data from the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) trial independently confirmed the relation between time to thrombolytic therapy and risk of cardiac rupture (p = 0.03). Analysis of 4,692 deaths in 44,346 patients demonstrated that the odds ratio of death was also directly correlated with time to treatment (p = 0.006); at 3 h, the odds ratio for death was 0.72 (0.67 to 0.77); at 14 h, it was 0.88 (0.77 to 1.00) and at 21 h, it was 1 (0.82 to 1.37). Thrombolytic therapy early after acute myocardial infarction improves survival and decreases the risk of cardiac rupture. Late administration of thrombolytic therapy also appears to improve survival but may increase the risk of cardiac rupture.

Left ventricular pseudoaneurysm.

Left ventricular (LV) pseudoaneurysms form when cardiac rupture is contained by adherent pericardium or scar tissue. Although LV pseudoaneurysms are not common, the diagnosis is difficult and they are prone to rupture. We evaluated the clinical presentation, diagnostic accuracy of imaging modalities, results of therapy and prognosis of 290 patients with LV pseudoaneurysms. Most cases of LV pseudoaneurysm were related to myocardial infarction (particularly inferior wall myocardial infarction) and cardiac surgery. Congestive heart failure, chest pain and dyspnea were the most frequently reported symptoms, but >10% of patients were asymptomatic. Physical examination revealed a murmur in 70% of patients. Almost all patients had electrocardiographic abnormalities, but these were usually nonspecific ST segment changes; only 20% of patients had ST segment elevation. Although radiographic findings were also usually nonspecific, the appearance of a mass was present in more than one half of patients and may be an important clue to the correct diagnosis. Left ventricular angiography was the most definitive test and can be useful in planning surgery since concomitant coronary angiography can be performed. Regardless of treatment, patients with LV pseudoaneurysms had a high mortality rate, especially those who did not undergo surgery. Because the symptoms, signs, electrocardiographic abnormalities and radiographic findings seen in patients with LV pseudoaneurysms can be indistinguishable from those in patients with coronary disease alone, a high clinical index of suspicion is needed to avoid missing the diagnosis.

Previous angina reduces in-hospital death in patients with acute myocardial infarction.

There is little information on how previous angina influences in-hospital deaths secondary to acute myocardial infarction (MI). This study evaluated the causes of in-hospital deaths in MI patients with and without previous angina. A total of 2,264 consecutive patients were admitted to our hospital due to acute MI. These patients were divided into 2 groups according to the presence or absence of prior MI. Both groups were further divided according to the presence or absence of previous angina. The causes of in-hospital deaths were classified into 4 categories: (1) cardiogenic shock or congestive heart failure, (2) cardiac rupture, (3) arrhythmia, and (4) other causes. In patients with a first MI, the in-hospital mortality rate was lower in patients with previous angina than those without (6.9% vs 11.4%, p <0.01). There was no significant difference between these patients with and without previous angina in in-hospital deaths due to cardiogenic shock or congestive heart failure, arrhythmia, or other causes. Death due to cardiac rupture was less frequent in patients with previous angina (1.4% vs 5.0%, p <0.01). In patients with prior MI, the in-hospital mortality rate was lower in patients with than without previous angina (17.7% vs 25.3%, p <0.05). In contrast to patients with their first MI, there was a trend toward a lower incidence of in-hospital death due to cardiogenic shock or congestive heart failure in patients with previous angina (12.8% vs 19.0%, p = 0.05). There were no significant differences in in-hospital deaths due to cardiac rupture, arrhythmia, and other causes between the 2 subgroups. In multivariate analysis, previous angina was an independent predictor of in-hospital death. Thus, in-hospital deaths after acute MI in patients with previous angina were less because of less cardiac rupture in patients with a first MI and less cardiogenic shock or congestive heart failure in patients with prior MI.

The role of two-dimensional echocardiography in coronary artery disease: a critical appraisal.

Coronary artery disease and its sequelae are the most common problems in the current practice of cardiology and internal medicine. Two-dimensional echocardiography, a relatively new technique, has already demonstrated its usefulness in the diagnosis of congenital and valvular heart disease, sometimes replacing catheterization as the diagnostic method of choice. This report critically reviews the usefulness of two-dimensional echocardiography in evaluating the patient with coronary artery disease and its complications. Four general areas are considered: myocardial infarction, complications of myocardial infarction, visualization of coronary arteries, and assessment of left ventricular function.

Mitral regurgitation due to ruptured chordae tendineae. Early and late results of valve repair.

From 1958 through 1980, 131 patients had repair of ruptured chordae tendineae of the mitral valve; 62% were men. Ages ranged from 5 to 70 years (median 57). Chordae to the anterior mitral leaflet were ruptured in 44 patients (34%), to the posterior mitral leaflet in 85 (65%), and to both leaflets in two patients (1%). The mitral valve was repaired by leaflet plication without resection in 116 patients, plication after wedge resection of the unsupported leaflet in six, Ivalon sponge buttress of the posterior leaflet in three, resuspension of chordae in two, and annuloplasty alone in the remaining four. Mitral valve annuloplasty was performed in addition to leaflet repair in 115 patients (88%). Operative (less than 30 days) mortality was 6.1%. Survival rate of patients dismissed from the hospital was 92% at 5 years and 73% at 10 years. There were no differences in late survival or risk of reoperation for recurrent or residual mitral insufficiency between patients with ruptured chordae to the anterior leaflet and those with ruptured chordae to the posterior leaflet. Survival was significantly better for the group with repair than it was for a group that underwent mitral valve replacement for ruptured chordae during this same time interval (5 year survival rate, 92% versus 72%, p less than 0.003). The incidence of thromboembolism after repair was 1.8 episodes/100 patient-years compared with 8.0 episodes/100 patient-years after replacement. Our data indicate that valvuloplasty is the procedure of choice for most patients with mitral regurgitation owing to ruptured chordae tendineae, including selected patients with ruptured chordae to the anterior leaflet.