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.

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.

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.

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.

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.

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.

Left atrial rupture secondary to myxomatous mitral valve disease in 11 dogs.

The purpose of this retrospective study was to evaluate the long-term outcome in dogs with left atrial rupture secondary to myxomatous mitral valve disease. Eleven client-owned dogs met the inclusion criteria for the study. Median age was 11.6 yr (range, 8.3-17.8 yr), and median weight was 5.8 kg (range, 3.8-15.2 kg). Of the 11 dogs, 10 survived the initial 24 hr after diagnosis and 5 of the dogs were still alive at the conclusion of data collection. The median survival of all dogs was 203 days. Dogs with no previous history of congestive heart failure (CHF) at the time of diagnosis had a significantly longer median survival time (345 days) compared with dogs with a previous history of CHF (160 days, P = 0.0038). Outcome of dogs with myxomatous mitral valve disease presenting with left atria rupture was more favorable than previously reported, and dogs without previous CHF survived the longest.

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.

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.

Cardiac rupture in takotsubo cardiomyopathy: a systematic review.

BACKGROUND: Takotsubo cardiomyopathy (TSC) and its complications, such as cardiac rupture (CR), are increasingly being reported in the literature. CR is associated with rapid clinical decline and is uniformly fatal if not surgically repaired. To identify patients who developed CR we performed an analysis of all available indexed cases in the literature and compared them with a control group of patients with TSC without rupture. HYPOTHESIS: Takotsubo cardiomyopathy patients with cardiac rupture do not differ significantly from those without rupture. METHODS: MEDLINE (2009) was searched for all TSC case reports with CR. Eleven case reports were identified. Using a random sampling method, we selected 12 case reports of TSC without rupture (control). We included our patient with TSC with rupture as the 12th case of TSC cohort with CR (CR group). Demographic and clinical characteristics were compared between CR group and control. RESULTS: All patients in the TSC group with rupture were female and were significantly older than controls. TSC group with rupture had significantly higher frequency of ST elevation in lead II and absence of T-wave inversion in lead V5 on hospital admission than controls. Mean ejection fraction, systolic blood pressure, and double product, a measure of oxygen demand, was significantly higher in the rupture group compared to controls. The CR group was associated with less frequent use of ß-blocker as compared to controls. CONCLUSIONS: CR as a complication of TSC could be more common than recognized. Higher double product and ejection fraction suggest higher fluctuation of intracardiac pressure and may cause CR in TSC. Use of ß blockers in TSC may provide protection against CR.

Efficacy of invasive treatment and the occurrence of cardiac rupture in acute ST-elevation myocardial infarction.

BACKGROUND: Cardiac rupture is a rare but potentially lethal complication of acute myocardial infarction with ST-elevation (STEMI). Primary percutaneous coronary intervention (pPCI) is a preferable treatment method of acute STEMI. Reperfusion at vascular and myocardial levels may be the key parameters determining probability of cardiac rupture. AIM: To analyse the relationship between reperfusion parameters and cardiac rupture occurrence in a group of patients with STEMI treated with pPCI. METHODS: Twenty three patients with cardiac rupture were selected out of 2800 patients with acute STEMI hospitalised and treated with pPCI from 2000 to 2007. Free wall or interventricular septum rupture was diagnosed on echocardiography or autopsy. The control group consisted of 255 patients with STEMI and pPCI treatment, but without cardiac rupture. The TIMI flow score was used to assess blood flow in an infarct-related artery (IRA). Myocardial perfusion was evaluated with the use of the myocardial blush grade (MBG) score. RESULTS: Female gender accounted for 47.8% of patients with cardiac rupture. Mean age was 72.9 ± 4.8 years for women and 64.3 ± 11.5 years for men. In 12 (52%) patients anterior descending artery was the IRA. Before the pPCI, the average blood flow in IRA was significantly lower in patients with subsequent cardiac rupture (0.41 ± 0.59) than in the reference group (0.81 ± 1.15; p < 0.05), and remained lower after pPCI (1.96 ± 0.93 in comparison to 2.93 ± 0.36; p < 0.05). Adequate blood flow (TIMI 3) was achieved only in 30.4% (7) of patients with cardiac rupture and in 95.3% (243) of the control group (p < 0.05). Myocardial tissue perfusion, assessed by MBG, was also lower (0.76 ± 1 vs 1.92 ± 1.13; p < 0.05). In-hospital mortality in patients with cardiac rupture reached 56.5% (13 subjects) compared to 3 (1.2%) patients in the reference group (p < 0.05). Multivariable analysis confirmed independent effects of lower TIMI and MBG after PCI as well as female gender on the occurrence of cardiac rupture. CONCLUSIONS: Poorer blood flow in IRA and worse tissue microvascular perfusion after pPCI are important risk factors of cardiac rupture occurrence in patients with STEMI.

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.

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.

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.

Surgical treatment for postinfarction left ventricular free wall rupture.

BACKGROUND: Left ventricular (LV) free wall rupture is a catastrophic complication after acute myocardial infarction. The optimal therapeutic strategy is controversial and the midterm results are unknown. METHODS: Between June 1993 and May 2006, 32 patients with an average age of 73 years (range, from 55 to 96 years) were surgically treated for LV free wall rupture. Sutureless technique (gluing autologous patch to the tear) was applied in all patients. RESULTS: The interval between acute myocardial infarction and the rupture was 33 +/- 42 hours and the interval between the rupture and the operation was 3.6 +/- 2.6 hours. Preoperatively, cardiopulmonary resuscitation was performed in eight cases. Percutaneous cardiopulmonary support was placed in six cases and intraaortic balloon pumping in 20 cases preoperatively. The in-hospital mortality was 15.6%. Two patients died of rerupture within ten days. While there was no rerupture during the follow-up period, five patients developed dyskinetic LV aneurysm and one patient developed LV pseudoaneurysm. CONCLUSIONS: The sutureless technique is a simple and effective option for the surgical treatment for LV free wall rupture. The preoperative moribund condition was highly associated with the operative mortality.

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.

[Features of tanatogenesis and extensiveness of myocardial infarction depending on severity of atherosclerotic stenosis of the coronary arteries]. / Osobennosti tanatogeneza i obshirnost' infarkta miokarda v zavisimosti ot rasprostranennosti ateroskleroticheskogo stenozirovaniia koronarnykh arterii.

142 fatal cases of acute myocardial infarction (AMI) are analyzed. In 56% cases the surface of AMI exceeded 50% of the working surface of the left ventricle and patients died, as a rule, during the first week of the disease of cardiogenic shock or progressing heart failure. In cases of a small AMI (up to 30% of working surface of the left ventricle, 25% cases) the frequent cause of death was external cardiorrhexis. It is emphasized that the size of AMI is not always determined by severity of stenosing atherosclerosis in the coronary arteries since isolated stenosis of one branch can also provoke a large AMI. The results are in favour of more active use of prophylactic surgical (including endovascular) treatment of ishemic heart disease before the development of a large AMI.

Estrogen and testosterone have opposing effects on chronic cardiac remodeling and function in mice with myocardial infarction.

Premenopausal women are much less prone to develop cardiovascular disease than men of similar age, but this advantage no longer applies after menopause. We previously found that male mice have a significantly higher rate of cardiac rupture than females during the acute phase of myocardial infarction (MI); however, the effects of sexual hormones on chronic remodeling are unknown. We hypothesized that estrogen (E) may protect the heart from chronic remodeling and deterioration of function post-MI, whereas testosterone (T) may have adverse effects. Mice (4 wk old) of both genders were divided into four groups: female groups consisted of 1) sham ovariectomy (S-Ovx) + placebo (P) (S-Ovx + P), 2) S-Ovx + T, 3) Ovx + P, and 4) Ovx + T; and male groups consisted of 1) sham castration (S-Cas)+ P (S-Cas + P), 2) S-Cas + 17beta-estradiol (E), 3) Cas + P, and 4) Cas + E. MI was induced 6 wk later. Echocardiography was performed to assess cardiac function and left ventricular dimensions (LVD). Myocyte cross-sectional area (MCSA) was measured at the end of the study. In females, both testosterone and ovariectomy decreased ejection fraction (EF) and increased LVD, and when combined they aggravated cardiac function and remodeling further. Testosterone significantly increased MCSA. In males, castration or estrogen increased EF and reduced LVD, whereas castration significantly reduced MCSA. Our data suggest that estrogen prevents deterioration of cardiac function and remodeling after MI, but testosterone worsens cardiac dysfunction and remodeling and has a pronounced effect when estrogen levels are reduced.