New Clinical Classification for Ventricular Free Wall Rupture following Acute Myocardial Infarction.

Ventricular free wall rupture (FWR) is a catastrophic complication after acute myocardial infarction (AMI). However, patients with FWR die of cardiac tamponade secondary to intrapericardial hemorrhage that can be treated if properly diagnosed. Unfortunately, FWR was still not diagnosed and classified quickly and accurately. The aim of this study was to present a new clinical classification for FWR. Seventy-eight patients with FWR after STEMI were enrolled in the study. We classified FWR, according to clinical situations after onset, into the cardiac arrest type, unstable type, and stable type. The cardiac arrest type was the most common type, accounting for about 83.3%. 90.8% of patients of this type were complicated with electromechanical dissociation at the time of FWR onset, and 100% of patients of this type died in the hospital. The unstable type was characterized by sudden clinical condition changes with moderate/massive pericardial effusion. In this study, 9.0% of patients were diagnosed as the unstable type. The average time from onset to death was 4.5 hours. This period was the "golden time" to rescue such patients. The stable types usually have stable hemodynamics, but may worsen, requiring rigorous detection of pericardial effusion and vital signs. In this study, 7.7% of patients were diagnosed as the stable type, and 83.5% of them survived in the hospital. The new clinical classification provides a basis for clinical diagnosis and treatment of FWR. The clinical application of the new classification is expected to improve the prognosis of FWR patients.

Cardiac rupture complicating acute myocardial infarction: the clinical features from an observational study and animal experiment.

BACKGROUND: Cardiac rupture (CR) is a fatal complication of ST-elevation myocardial infarction (STEMI) with its incidence markedly declined in the recent decades. However, clinical features of CR patients now and the effect of reperfusion therapy to CR remain unclear. We investigated the clinical features of CR in STEMI patients and the effect of reperfusion therapy to CR in mice. METHODS: Two studies were conducted. In clinical study, data of 1456 STEMI patients admitted to the First Hospital, Xi'an Jiaotong University during 2015.12. ~ 2018.12. were analyzed. In experimental study, 83 male C57BL/6 mice were operated to induce MI. Of them, 39 mice were permanent MI (group-1), and remaining mice received reperfusion after 1 h ischemia (21 mice, group-2) or 4 h ischemia (23 mice, group-3). All operated mice were monitored up to day-10. Animals were inspected three times daily for the incidence of death and autopsy was done for all mice found died to determine the cause of death. RESULTS: CR was diagnosed in 40 patients: free-wall rupture in 17, ventricular septal rupture in 20, and combined locations in 3 cases. CR presented in 19 patients at admission and diagnosed in another 21 patients during 1 ~ 14 days post-STEMI, giving an in-hospital incidence of 1.4%. The mortality of CR patients was high during hospitalization accounting for 39% of total in-hospital death. By multivariate logistic regression analysis, older age, peak CK-MB and peak hs-CRP were independent predictors of CR post-STEMI. In mice with non-reperfused MI, 17 animals (43.6%) died of CR that occurred during 3-6 days post-MI. In MI mice received early or delayed reperfusion, all mice survived to the end of experiment except one mouse died of acute heart failure. CONCLUSION: CR remains as a major cause of in-hospital death in STEMI patients. CR patients are characterized of being elderly, having larger infarct and more server inflammation. Experimentally, reperfusion post-MI prevented CR.

Clinical Manifestation, Timing Course, Precipitating Factors, and Protective Factors of Ventricular Free Wall Rupture Following ST-Segment Elevation Myocardial Infarction.

Ventricular free wall rupture (FWR) is a catastrophic complication of that occurs after acute myocardial infarction (AMI), and at present, its clinical characteristics are unclear. We analyzed a total of 6,712 consecutive patients who presented with ST-segment elevation myocardial infarction (STEMI), and 78 patients with FWR after STEMI were enrolled in the study. Patients' demographic data, clinical manifestation, laboratory test results, and angiographic features were then collected and analyzed. FWR occurred in 78 cases (1.16%), and the inhospital mortality of FWR was up to 92.3%. Among the 78 FWR patients, 72 obtained accurate rupture time. FWR typically occurred within the first week after the infarct. Compared to late-phase FWR (more than 48 hours after STEMI) patients, early-phase FWR (during 48 hours after STEMI) patients showed significantly higher random glucose and higher percentage of anterior myocardial infarction. Besides, dual antiplatelet therapy (DAPT), ß-blockers, and angiotensin-converting enzyme inhibitors/angiotensin receptor blocker (ACEI/ARB) were used less frequently in early-phase FWR patients. Moreover, we first reported the precipitating factors of FWR. Defecating, transporting, acute emotional upset, diets, and invasive treatment turned out to be the main triggers for FWR. Furthermore, we found that patients who survived from FWR were younger, had higher ß-blocker coverage in the inhospital treatment, and had a higher frequency of primary PCI. FWR remains an infrequent but devastating complication of STEMI. We have found several factors related to the occurrence and prognosis of FWR. This study provides evidence for a better understanding of FWR.

Combination of eosinophil percentage and high-sensitivity C-reactive protein predicts in-hospital major adverse cardiac events in ST-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention.

BACKGROUND: Eosinophil levels predict prognosis in ST-segment elevation myocardial infarction (STEMI) patients. Both eosinophils and high-sensitivity C-reactive protein (hs-CRP) play a major role in the acute inflammatory response of myocardial infarction. The purpose of this study was to evaluate eosinophil percentage (EOS%) and hs-CRP as prognostic markers for in-hospital adverse events in STEMI patients undergoing primary percutaneous coronary intervention. METHODS: We retrospectively analyzed the clinical data of 518 patients. Major adverse cardiac events (MACEs) were defined as cardiac rupture, cardiac arrest, malignant arrhythmia, and cardiac death. Based on the receiver operating characteristic (ROC) analysis, all patients were regrouped into 3 groups (None, One, and Two) according to cutoff EOS% value (≤0.3%) and hs-CRP value (>11.8 mg/L). Both Cox regression analyses and the KM (Kaplan-Meier) survival curve were used to examine the prognostic role of combined hs-CRP and EOS% in cardiovascular events. RESULTS: Of the 518 STEMI patients, 50 of them developed MACEs. Patients who developed MACEs had a significantly lower EOS% and higher hs-CRP than patients who remained MACE-free. In the multivariable Cox regression analysis, the highest risk of in-hospital MACEs was constantly observed in patients with a combined low EOS% and elevated hs-CRP. Patients with reduced EOS% and high hs-CRP had significantly higher incidence rates of cardiac rupture (P = .001), cardiac arrest (P = .001), and malignant arrhythmia (P < .001); furthermore, they had the worst cumulative survival compared with the other two groups. CONCLUSION: Combined reduced EOS% and elevated hs-CRP were valuable tools for identifying patients at risk of in-hospital MACEs.

A multicenter study on the clinical characteristics and risk factors of in-hospital mortality in patients with mechanical complications following acute myocardial infarction.

Mechanical complications (MCs) following acute myocardial infarction (AMI), such as ventricular septal rupture (VSR), free-wall rupture (FWR), and papillary muscle rupture (PMR), are fatal. However, the risk factors of in-hospital mortality among patients with MCs have not been previously reported in Japan. The purpose of this study was to evaluate the prognostic factors of in-hospital mortality in these patients. The study cohort consisted of 233 consecutive patients with MCs from the registry of 10 facilities in the Cardiovascular Research Consortium-8 Universities (CIRC-8U) in East Japan between 1997 and 2014 (2.3% of 10,278 AMI patients). The authors conducted a retrospective observational study to analyse the correlation between the subtypes of MCs with in-hospital mortality, clinical data, and medical treatment. We observed a decreasing incidence of MC (1997-2004: 3.7%, 2005-2010: 2.1%, 2011-2014: 1.9%, p < 0.001). In-hospital mortality among patients with MCs was 46%. Thirty-three percent of patients with MCs were not able to undergo surgical repair due to advanced age or severe cardiogenic shock. In-hospital mortality among patients who had undergone surgical repair was 29% (VSR: 21%, FWR: 33%, PMR: 60%). In patients with MCs, hazard ratio for in-hospital mortality according to multivariate analysis of without surgical repair was 5.63 (95% CI 3.54-8.95). In patients with surgical repair, the hazard ratios of blow-out-type FWR (5.53, 95% confidence interval (CI) 2.22-13.76), those with renal dysfunction (3.11, 95% CI 1.37-7.05), and those receiving venoarterial extracorporeal membrane oxygenation (VA-ECMO) (3.79, 95% CI 1.81-7.96) were significantly high. Although primary percutaneous coronary intervention (PCI) is associated with decreased incidence of MCs, high in-hospital mortality persisted in patients with MCs that also presented with renal dysfunction and in those requiring VA-ECMO. Early detection and surgical repair of MCs are essential.

Temporal Trends and Outcomes of Mechanical Complications in Patients With Acute Myocardial Infarction.

OBJECTIVES: The aim of this study was to examine the temporal trends and outcomes of mechanical complications after myocardial infarction in the contemporary era. BACKGROUND: Data regarding temporal trends and outcomes of mechanical complications after ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) are limited in the contemporary era. METHODS: The National Inpatient Sample database (2003 to September 2015) was queried to identify all STEMI and NSTEMI hospitalizations. Temporal trends and outcomes of mechanical complications after STEMI and NSTEMI, including papillary muscle rupture, ventricular septal defect, and free wall rupture, were described. RESULTS: The analysis included 3,951,861 STEMI and 5,114,270 NSTEMI hospitalizations. Mechanical complications occurred in 10,726 of STEMI hospitalizations (0.27%) and 3,041 of NSTEMI hospitalizations (0.06%), with no changes in trends (p = 0.13 and p = 0.83, respectively). The rates of in-hospital mortality in patients with mechanical complications were 42.4% after STEMI and 18.0% after NSTEMI, with no significant trend changes (p = 0.62 and p = 0.12, respectively). After multivariate adjustment, patients who had mechanical complications after myocardial infarction had higher in-hospital mortality, cardiogenic shock, acute kidney injury, hemodialysis, and respiratory complications compared with those without mechanical complications. Predictors of lower mortality in patients with mechanical complications who developed cardiogenic shock included surgical repair in the STEMI and NSTEMI cohorts and percutaneous coronary intervention in the STEMI cohort. CONCLUSIONS: Contemporary data from a large national database show that the rates of mechanical complications are low in patients presenting with STEMI and NSTEMI. Post-myocardial infarction mechanical complications continue to be associated with high mortality rates, which did not improve during the study period.

Clinical and echocardiographic presentation of postmyocardial infarction papillary muscle rupture.

BACKGROUND: Severe mitral regurgitation (MR) can occur following myocardial infarction (MI) with either partial or complete papillary muscle rupture (pPMR or cPMR). Although the incidence of this complication has significantly decreased, it is still associated with significant mortality. We sought to evaluate the different echocardiographic and clinical presentations of pPMR and cPMR. METHODS AND RESULTS: A review of all the urgent procedures for ischemic MR between January 2000 and June 2016 was performed to identify patients who underwent surgery for PMR. Surgical protocols and echocardiographic studies were used to identify patients with cPMR and pPMR. A total of 37 patients had cardiac surgery for PMR (18 cPMR, 19 pPMR). All patients with cPMR were in cardiogenic shock at the time of diagnosis, as opposed to only 53% of patients with pPMR (P = 0.0008). Between the time of diagnosis and surgery, 7 patients with pPMR developed cardiogenic shock. Transthoracic echocardiography (TTE) led to the diagnosis in 72% of cPMR and 32% of pPMR (P = 0.02). TEE had a yield of 100% for both cPMR and pPMR. Six pathologic varieties of post-MI PMR were recognized on echocardiography and during surgery. Early postoperative, 1 (72% vs 84%), 3 (67% vs 84%), and 5 years (67% vs 74%) survival rates were similar for cPMR and pPMR (P = 0.26). CONCLUSIONS: Partial PMR is associated with a different clinical and echocardiographic presentation than cPMR. Still, most pPMR patients progress toward cardiogenic shock. Prompt diagnosis and referral for surgery are critical and could potentially decrease mortality.

Rotura miocárdica de ventrículo izquierdo secundaria a infarto agudo de miocardio / Myocardial rupture of left ventricle secondary to myocardial infarction

Fundamento: la rotura miocárdica es una complicación rara del infarto agudo de miocardio con una incidencia global de alrededor del 6,2 porciento. Objetivo: caracterizar los fallecidos por infarto agudo de miocardio con la rotura de pared de ventrículo izquierdo. Métodos: se realizó un estudio retrospectivo, descriptivo y observacional, en el cual se analizaron los fallecidos con diagnóstico de causa directa de muerte: taponamiento cardíaco por hemopericardio, rotura de miocardio e infarto agudo de miocardio. Resultados: de 877 infartos agudos de miocardio diagnosticados entre 2010 a 2018, 16 de ellos presentaron rotura de pared miocárdica de los cuales 68,8 porciento eran del masculino. El hábito de fumar fue el factor de riesgo predominante. Solo en un 35,7 porciento se realizó el diagnóstico clínico correcto de IAM y en ninguno de los casos fue planteado el diagnóstico de rotura de miocardio o taponamiento cardíaco por hemopericardio. La región anatómica del corazón donde con mayor frecuencia se localizaron las roturas de miocardio fue en la pared posterior. Conclusiones: la rotura de la pared de miocardio es una complicación del infarto poco frecuente pero catastrófica con una mortalidad elevada, sin embargo, esta puede reducirse si el cuadro clínico es sospechado, y se realiza un diagnóstico precoz con instauración de medidas de apoyo para mantener la estabilidad hemodinámica(AU)

Background: myocardial rupture is a rare complication of acute myocardial infarction with an overall incidence of around 6.2 percent. Objective: to characterize the deaths due to acute myocardial infarction with the rupture of the left ventricle wall. Methods: a retrospective, descriptive and observational study was carried out in which the deceased were analyzed with a diagnosis of direct cause of death: cardiac tamponade due to hemopericardium, myocardial rupture and acute myocardial infarction.Results: of 877 acute myocardial infarcts diagnosed between 2010 and 2018, 16 of them had myocardial wall rupture of which 68.8 percent were male. The habit of smoking was the predominant risk factor. Only in 35.7 percent the correct clinical diagnosis of AMI was made and in none of the cases was the diagnosis of myocardial rupture or cardiac tamponade due to hemopericardium. The anatomical region of the heart where myocardial ruptures were most frequently located was in the posterior wall.Conclusions: rupture of the myocardial wall is a rare but catastrophic complication of infarction with a high mortality, however, this can be reduced if the clinical picture is suspected, and an early diagnosis is made with the introduction of support measures to maintain hemodynamic stability(AU)

Sutureless repair for postinfarction left ventricular free wall rupture.

OBJECTIVE: Left ventricular free wall rupture is a catastrophic complication of acute myocardial infarction. Sutureless repair has been reported to be an effective surgical procedure for left ventricular free wall rupture. However, the outcomes of sutureless repair remain unclear. METHODS: Between January 2001 and December 2016, 42 patients were treated for left ventricular free wall rupture at Jichi Medical University. Of them, 35 consecutive patients undergoing sutureless repair using the TachoComb (CSL Behring, Tokyo, Japan) or TachoSil (Nycomed, Zurich, Switzerland) patches were included in this study. No patient required cardiopulmonary bypass. The oozing type of left ventricular free wall rupture was observed in 33 patients (94%), and the blow-out type was observed in 2 patients (6%). The rupture sites were the anterior wall in 16 patients (46%), the posterior-lateral wall in 11 patients (31%), and the inferior wall in 8 patients (23%). RESULTS: The in-hospital mortality rate was 17% (6 patients). Re-rupture after sutureless repair occurred in 17% (6 patients). Of them, 4 cases (67%) of re-rupture occurred within 24 hours after surgery. The 2 patients with blow-out type left ventricular free wall rupture experienced re-rupture. Three patients required mitral valve surgery after sutureless repair during the admission. The overall survivals at 1, 5, and 10 years were 71.4%, 68.6%, and 62.9%, respectively. Multivariable analysis revealed that re-rupture was an independent predictor for decreased survival (hazard ratio, 58.6; 95% confidence interval, 4.9-701.6; P = .001). Postoperative pseudoaneurysm formation was not detected during the follow-up. CONCLUSIONS: Sutureless repair using TachoComb/TachoSil patches can be a viable treatment option for left ventricular free wall rupture. Care should be taken when applying this technique in cases of the blow-out type left ventricular free wall rupture.

Comparison in Prevalence, Predictors, and Clinical Outcome of VSR Versus FWR after Acute Myocardial Infarction: The Prospective, Multicenter Registry MOODY Trial-Heart Rupture Analysis.

BACKGROUND: Differences in the predictors between ventricular septal rupture (VSR) and free wall rupture (FWR) have not been fully studied. Data on the prevalence and clinical outcome of heart rupture are limited. HYPOTHESIS: This study aimed to investigate heart rupture incidence and clinical results in patients with acute myocardial infarction (AMI). METHODS: Of 9265 AMI patients in the MOODY registry between March 1999 and October 2016, a total of 146 were studied. The primary clinical endpoint was rupture prevalence and in-hospital mortality. Independent factors of heart rupture were analyzed using Cox proportional model and were compared between patients with VSR and those with FWR. RESULTS: Of 9265 AMI patients, 146 (1.58%) patients had a heart rupture (FWR, 94 (1.02%)) and VSR (52 (0.56%)). All patients with FWR died during hospitalization, and in-hospital mortality was recorded in 37 (71.2%) patients with VSR, who had an extremely longer time delay from AMI onset to the first medical contact (FMC) (~20 h). FWR usually occurred in patients with ST-elevation myocardial infarction (STEMI) patients with a FMC ≥ 3 h, for whom primary reperfusion was not performed. Percutaneous repair at 1-2 weeks following AMI was associated with less mortality, and 9 of 38 patients who underwent non-primary reperfusion died post procedure. CONCLUSION: This study demonstrated the importance of shortening FMC to prevent VSR and of early primary reperfusion in STEMI patients to reduce FWR. Urgent closure of rupture is necessary to reduce in-hospital and 1-year mortality. CLINICAL TRIAL REGISTRATION: http://www.clinicaltrials.org, identifier: No. NCT03051048.

The necessity of conversion from coronary care unit to the cardiovascular intensive care unit required for cardiologists.

The in-hospital mortality rate of acute myocardial infarction (AMI) has dramatically decreased due to the treatment at the coronary care unit (CCU), especially with the progress of arrhythmia therapy and reperfusion therapy. On the other hand, severe heart failure and multiple organ failure are increasing due to aging populations and multiple organ diseases. As a result, patients with AMI without complications are less likely to be admitted to the CCU, and cardiologists staying in the CCU have also decreased. The mortality rate is high when complications such as cardiogenic shock, cardiac rupture, and in-hospital cardiac arrest occur in AMI, therefore careful intensive care even in low-risk AMI is necessary. For cardiologists, mechanical ventilation, renal replacement therapy, or infection control are necessary for cardiovascular intensive care, and integrated multidisciplinary care coordinated by skilled intensive care physicians, nurses, respiratory therapists, physiotherapists, pharmacists, nutritionists, social workers, and clinical engineers is important. Therefore, for the critical care of cardiovascular diseases, it is necessary to convert from CCU to the cardiovascular intensive care unit.

Mitral valve surgery for acute papillary muscle rupture.

BACKGROUND: Papillary muscle rupture (PMR) is a rare complication of a myocardial infarction. The aim of this study was to review our results of mitral valve surgery for acute PMR. METHODS: Data from patients undergoing emergent mitral valve surgery for acute PMR between 2011 and 2017 at our institution were reviewed. Outcomes included operative morbidity and mortality, mitral valve reoperation, and hospital readmission. RESULTS: A total of 2479 patients underwent mitral valve surgery during the study period including 24 (1.0%) for PMR. Mean age was 62 years, and two (8.3%) patients had prior open-heart surgery. Overall Society of Thoracic Surgeons predicted risk of mortality was 17.5%. Operative mortality was 12.5% (n = 3) with an observed-to-expected mortality ratio of 0.71. There were no strokes, and new onset dialysis was required in two (8.3%) patients. Mean follow-up was 2.40 ± 1.96 years. Three-year mortality, mitral valve reoperation, and readmission rates were 21.1%, 5.0%, and 45.4%. CONCLUSIONS: Expeditious operative intervention for PMR can be associated with acceptable operative and longer-term outcomes.

Association of the SYNTAX Score II with cardiac rupture in patients with ST-segment elevation myocardial infarction undergoing a primary percutaneous coronary intervention.

BACKGROUND: Despite advances in reperfusion strategies, medical therapy, and emergent surgery, cardiac rupture (CR) is still a major lethal complication. Numerous parameters have been found to be associated with CR development after a primary percutaneous coronary intervention (pPCI). SYNTAX Score (SS) and SYNTAX Score II (SSII) have been studied in ST-segment elevation myocardial infarction (STEMI) patients, and higher scores have been associated with higher mortality. However, the relationship between CR and SSII is unclear. This study investigates the possible relationship between CR and SS, SSII in STEMI patients treated with pPCI. PATIENTS AND METHODS: We enrolled 1663 consecutive STEMI patients treated with pPCI, who were divided into two groups according to CR development and compared with each other. Patients were further stratified into the three groups according to their SSII values. RESULTS: In this study, 33 (1.98%) patients developed CR. Both SS and SSII of those with CR were significantly higher than those without (19.27±4.0 vs. 16.40±4.55; P<0.001 and 49.40±16.54 vs. 30.92±11.80; P<0.001, respectively). It was also observed that CR increased gradually according to increasing SSII tertiles. SSII was found to be an independent predictor for CR (odds ratio=1.043, 95% confidence interval: 1.012-1.074; P=0.006). In the long-term follow-up, all-cause mortality was significantly higher in patients with CR than those without (60.6 vs. 8.8%; P<0.001). CONCLUSION: This study shows that SSII is an independent predictor for CR. Furthermore, patients with CR were associated with a poor prognosis. Closer follow-up of patients with high SSII may be useful in the early detection and treatment of this fatal complication.

Development and validation of clinical risk score to predict the cardiac rupture in patients with STEMI.

BACKGROUND: Cardiac rupture (CR) is a fatal complication of ST-elevation myocardial infarction (STEMI) with poor prognosis. The aim of this study was to develop and validate practical risk score to predict the CR after STEMI. METHODS: A total of 11,234 STEMI patients from 7 centers in China were enrolled in our study, we firstly developed a simplified fast-track CR risk model from 7455 STEMI patients, and then prospectively validated the CR risk model using receiver-operating characteristic (ROC) curves by the other 3779 consecutive STEMI patients. This trial is registered with ClinicalTrials.gov, number NCT02484326. RESULTS: The incidence of CR was 2.12% (238/11,234), and the thirty-day mortality in CR patients was 86%. We developed a risk model which had 7 independent baseline clinical predictors (female sex, advanced age, anterior myocardial infarction, delayed admission, heart rate, elevated white blood cell count and anemia). The CR risk score system differentiated STEMI patients with incidence of CR ranging from 0.2% to 13%. The risk score system demonstrated good predictive value with area under the ROC of 0.78 (95% CI 0.73-0.84) in validation cohort. Primary percutaneous coronary intervention decreased the incidence of CR in high risk group (3.9% vs. 6.2%, p<0.05) and very high risk group (8.0% vs. 15.2%, p<0.05). CONCLUSIONS: A simple risk score system based on 7 baseline clinical variables could identify patients with high risk of CR, for whom appropriate treatment strategies can be implemented.

Rotura cardíaca como complicación de un infarto agudo de miocardio / Cardiac rupture as a complication of acute myocardial infarction

Introducción: Las principales causas de fallecimiento en pacientes con infarto miocárdico son las arritmias cardíacas y las complicaciones mecánicas; dentro de ellas, la rotura cardíaca provoca un grave deterioro hemodinámico con una elevada mortalidad. Objetivo: caracterizar los pacientes fallecidos por rotura cardíaca como complicación de un infarto agudo de miocardio. Método: Estudio descriptivo, transversal, en el Hospital Universitario Arnaldo Milián Castro de Santa Clara, Cuba, entre 2010 y 2014. Se estudiaron todos los pacientes que fallecieron con diagnóstico clínico de infarto agudo de miocardio, a los que se les realizó autopsia y se confirmó una rotura cardíaca. Resultados: Predominaron el sexo femenino (53,2 por ciento), la edad avanzada (más de 75 años), el hábito de fumar (64,5 por ciento), la hipertensión arterial (61,3 por ciento) y la ausencia de angina (96,8 por ciento). En 43 pacientes (69,4 por ciento) no se utilizó trombólisis, 31 de ellos (72,1 por ciento) tuvieron una forma de presentación atípica del infarto. La rotura de la pared libre del ventrículo izquierdo (91,9 por ciento) fue la más frecuente. Se identificó taponamiento cardíaco en el 80,7 por ciento de los pacientes y shock cardiogénico en 7,7 por ciento. Casi la mitad de los que presentaron rotura de la pared libre (47,3 por ciento) tuvieron un infarto anterior extenso. Conclusiones: Predominaron los pacientes del sexo femenino, mayores de 75 años, con hábito de fumar, hipertensión arterial y diabetes mellitus. La mayoría de los pacientes no tuvo angina previa, no recibió tratamiento trombolítico y mostró formas clínicas de presentación atípicas. La rotura de pared libre resultó la más frecuente y casi la mitad de quienes la sufrieron tenían un infarto anterior extenso(AU)

Morphological predictors for no reflow phenomenon after primary percutaneous coronary intervention in patients with ST-segment elevation myocardial infarction caused by plaque rupture.

AIMS: Myocardial no reflow after percutaneous coronary intervention (PCI) is associated with poor outcome. Patients with ST-segment elevation myocardial infarction (STEMI) caused by plaque rupture are at high risk for no reflow. However, specific morphologic characteristics associated with no reflow are unknown in this population. The aim of this study is to identify the morphological characteristics of culprit plaques associated with no reflow in patients with STEMI caused by plaque rupture using both optical coherence tomography (OCT) and intravascular ultrasound (IVUS). METHODS AND RESULTS: We enrolled 145 patients with STEMI who underwent both OCT and IVUS within 12 h of symptom onset. Among these patients, we excluded those with plaque erosion and calcified nodule and included 72 patients who had plaque rupture as an underlying mechanism for STEMI. Myocardial no reflow, defined as Thrombolysis in Myocardial Infarction flow grade 0-2 and/or myocardial blush grade 0-1 after PCI, was observed in 28 patients (38.9%). Onset to recanalization time was similar between the groups with and without no reflow. Receiver-operating curve analysis revealed OCT-derived lipid index > 3500 [area under curve (AUC) 0.77, P < 0.001] and IVUS-derived plaque burden > 81.5% (AUC 0.70, P = 0.002) were the best discriminators for myocardial no reflow. CONCLUSION: No reflow occurred in nearly 40% of patients with STEMI caused by plaque rupture. Large lipid index and plaque burden were critical morphological discriminators between no reflow and normal flow.

Toll-like receptor 9 prevents cardiac rupture after myocardial infarction in mice independently of inflammation.

We have reported that the Toll-like receptor 9 (TLR9) signaling pathway plays an important role in the development of pressure overload-induced inflammatory responses and heart failure. However, its role in cardiac remodeling after myocardial infarction has not been elucidated. TLR9-deficient and control C57Bl/6 wild-type mice were subjected to left coronary artery ligation. The survival rate 14 days postoperation was significantly lower in TLR9-deficient mice than that in wild-type mice with evidence of cardiac rupture in all dead mice. Cardiac magnetic resonance imaging showed no difference in infarct size and left ventricular wall thickness and function between TLR9-deficient and wild-type mice. There were no differences in the number of infiltrating inflammatory cells and the levels of inflammatory cytokine mRNA in infarct hearts between TLR9-deficient and wild-type mice. The number of α-smooth muscle actin (αSMA)-positive myofibroblasts and αSMA/Ki67-double-positive proliferative myofibroblasts was increased in the infarct and border areas in infarct hearts compared with those in sham-operated hearts in wild-type mice, but not in TLR9-deficient mice. The class B CpG oligonucleotide increased the phosphorylation level of NF-κB and the number of αSMA-positive and αSMA/Ki67-double-positive cells and these increases were attenuated by BAY1-7082, an NF-κB inhibitor, in cardiac fibroblasts isolated from wild-type hearts. The CpG oligonucleotide showed no effect on NF-κB activation or the number of αSMA-positive and αSMA/Ki67-double-positive cells in cardiac fibroblasts from TLR9-deficient hearts. Although the TLR9 signaling pathway is not involved in the acute inflammatory response in infarct hearts, it ameliorates cardiac rupture possibly by promoting proliferation and differentiation of cardiac fibroblasts.

Early citalopram treatment increases mortality due to left ventricular rupture in mice after myocardial infarction.

AIMS: Both anxiety and depression are common and independent outcome predictors in patients after myocardial infarction (MI). However, it is unclear whether and how anti-depressants influence remodeling after MI. Thus, we studied cardiac remodeling in mice after experimental MI under treatment with citalopram, a selective serotonin reuptake inhibitor widely used as antidepressant. METHODS AND RESULTS: Treatment with citalopram versus saline was applied via osmotic pump after coronary artery ligation. Two different groups were studied: early treatment during the healing phase (starting immediately after surgery), or late treatment in the remodeling phase (starting 7days after surgery). Late treatment did not change mortality or left ventricular remodeling after MI over the period of 6weeks. However, in the early treatment group mortality was increased in citalopram-treated mice predominantly due to left ventricle rupture without differences in infarct size. Remodeling 4weeks after MI was not altered by the treatment. Neither infiltration of inflammatory cells, as determined by FACS analysis of myocardial tissue, nor mRNA-expression of inflammatory cytokines changed 3days after MI in the early treatment group. However, extracellular matrix functioning was altered: There was a significant increase of MMP13 in citalopram treated animals after MI. Pretreatment with the MMP inhibitor PD 166793 prevented left ventricular ruptures and demonstrated a tendency to improved survival after citalopram treatment. CONCLUSIONS: Treatment with antidepressant citalopram in the acute but not in the late phase after MI significantly increased mortality in mice by disturbing early healing. Pharmacological MMP inhibition partially reversed the deleterious effects of citalopram.

Porphyromonas gingivalis, a periodontal pathogen, enhances myocardial vulnerability, thereby promoting post-infarct cardiac rupture.

There is a strong association between periodontal disease (PD) and atherosclerosis. However, it remains unknown whether PD is also involved in myocardial damage. We hypothesized that infection with periodontal pathogens could cause an adverse outcome after myocardial infarction (MI). C57BL/6J mice were inoculated with Porphyromonas gingivalis (P.g.), a major periodontal pathogen, or injected with phosphate-buffered saline (PBS) into a subcutaneously-implanted steelcoil chamber before and after coronary artery ligation. A significant increase in mortality, due to cardiac rupture, was observed in the P.g.-inoculated MI mice. Ultrastructural examinations revealed that P.g. invaded the ischemic myocardium of the P.g.-inoculated MI mice. The expression of p18 Bax, an active form of pro-apoptotic Bax protein, markedly increased in the P.g.-inoculated MI hearts. In vitro experiments demonstrated that gingipain, a protease uniquely secreted from P.g., cleaved wild type Bax at Arg34, as evidenced by the observation that the cleavage of Bax by gingipain was completely abolished by the Arg34Ala mutation in Bax. Treatment with immunoglobulin Y against gingipain significantly decreased the mortality of the P.g.-inoculated MI mice caused by cardiac rupture. Furthermore, inoculation of P.g. also resulted in an increase of MMP-9 activity in the post-MI myocardium by enhancing oxidative stress, possibly through impairing the selective autophagy-mediated clearance of damaged mitochondria. In conclusion, infection with P.g. during MI plays a detrimental role in the healing process of the infarcted myocardium by invasion of P.g. into the myocardium, thereby promoting apoptosis and the MMP-9 activity of the myocardium, which, in turn, causes cardiac rupture.

Akt-dependent Girdin phosphorylation regulates repair processes after acute myocardial infarction.

Myocardial infarction is a leading cause of death, and cardiac rupture following myocardial infarction leads to extremely poor prognostic feature. A large body of evidence suggests that Akt is involved in several cardiac diseases. We previously reported that Akt-mediated Girdin phosphorylation is essential for angiogenesis and neointima formation. The role of Girdin expression and phosphorylation in myocardial infarction, however, is not understood. Therefore, we employed Girdin-deficient mice and Girdin S1416A knock-in (Girdin(SA/SA)) mice, replacing the Akt phosphorylation site with alanine, to address this question. We found that Girdin was expressed and phosphorylated in cardiac fibroblasts in vitro and that its phosphorylation was crucial for the proliferation and migration of cardiac fibroblasts. In vivo, Girdin was localized in non-cardiomyocyte interstitial cells and phosphorylated in α-smooth muscle actin-positive cells, which are likely to be cardiac myofibroblasts. In an acute myocardial infarction model, Girdin(SA/SA) suppressed the accumulation and proliferation of cardiac myofibroblasts in the infarcted area. Furthermore, lower collagen deposition in Girdin(SA/SA) mice impaired cardiac repair and resulted in increased mortality attributed to cardiac rupture. These findings suggest an important role of Girdin phosphorylation at serine 1416 in cardiac repair after acute myocardial infarction and provide insights into the complex mechanism of cardiac rupture through the Akt/Girdin-mediated regulation of cardiac myofibroblasts.