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Background: The relation between ventricular arrhythmia and fibrosis in mitral valve prolapse (MVP) is reported, but underlying valve-induced mechanisms remain unknown. We evaluated the association between abnormal MVP-related mechanics and myocardial fibrosis, and their association with arrhythmia. Methods: We studied 113 patients with MVP with both echocardiogram and gadolinium cardiac magnetic resonance imaging for myocardial fibrosis. Two-dimensional and speckle-tracking echocardiography evaluated mitral regurgitation, superior leaflet and papillary muscle displacement with associated exaggerated basal myocardial systolic curling, and myocardial longitudinal strain. Follow-up assessed arrhythmic events (nonsustained or sustained ventricular tachycardia or ventricular fibrillation). Results: Myocardial fibrosis was observed in 43 patients with MVP, predominantly in the basal-midventricular inferior-lateral wall and papillary muscles. Patients with MVP with fibrosis had greater mitral regurgitation, prolapse, and superior papillary muscle displacement with basal curling and more impaired inferior-posterior basal strain than those without fibrosis ( P P 6-month follow-up developed ventricular arrhythmias associated (univariable) with fibrosis, greater prolapse, mitral annular disjunction, and double-peak strain. In multivariable analysis, double-peak strain showed incremental risk of arrhythmia over fibrosis. Conclusions: Basal inferior-posterior myocardial fibrosis in MVP is associated with abnormal MVP-related myocardial mechanics, which are potentially associated with ventricular arrhythmia. These associations suggest pathophysiological links between MVP-related mechanical abnormalities and myocardial fibrosis, which also may relate to ventricular arrhythmia and offer potential imaging markers of increased arrhythmic risk.

BackgroundProsthetic graft replacement of thoracic aortic aneurysms (TAA) yields benefits but risks persist in the native aorta, especially in Marfan syndrome (MFS). Differential biomechanics between chronically grafted and native aortic regions are unknown.MethodsFunctional cardiac magnetic resonance (cine-CMR) imaging was performed in non-surgical MFS patients (root or ascending diameter≤4.5cm) and patients after (>1 year) proximal grafting. Analyses included mid-ascending and -descending aortic size (diameter, area) and compliance indices, including global circumferential strain (GCS), fractional area change (FAC), stiffness index, and distensibility.Results46 MFS patients underwent cine-CMR, including 21 with chronic proximal grafts (10.5±7.3 years post-operatively). Patients with and without grafts had similar clinical and hemodynamic characteristics. Grafted and non-grafted ascending aortic size was similar between groups (p=NS), but functional parameters differed as evidenced by decrements in GCS, FAC, stiffness index, and distensibility (all pConclusionsMarfan syndrome patients with chronic proximal aortic grafts manifest distinct vessel wall biomechanics in grafted and native regions that differ from non-surgical comparators, including decreased strain (a marker of reduced compliance) within grafted territories and increased strain in native aortic regions distal to grafts.

The goal of this study was to test whether ischemia-mediated contractile dysfunction underlying the mitral valve affects functional mitral regurgitation (FMR) and the prognostic impact of FMR.FMR results from left ventricular (LV) remodeling, which can stem from myocardial tissue alterations. Stress cardiac magnetic resonance can assess ischemia and infarction in the left ventricle and papillary muscles; relative impact on FMR is uncertain.Vasodilator stress cardiac magnetic resonance was performed in patients with known or suspected coronary artery disease at 7 sites. Images were centrally analyzed for MR etiology/severity, mitral apparatus remodeling, and papillary ischemia.A total of 8,631 patients (mean age 60.0 ± 14.1 years; 55% male) were studied. FMR was present in 27%, among whom 16% (n = 372) had advanced (moderate or severe) FMR. Patients with ischemia localized to subpapillary regions were more likely to have advanced FMR (p = 0.003); those with ischemia localized to other areas were not (p = 0.17). Ischemic/dysfunctional subpapillary myocardium (odds ratio: 1.24/10% subpapillary myocardium; confidence interval: 1.17 to 1.31; p 0.001) was associated with advanced FMR controlling for infarction. Among a subgroup with (n = 372) and without (n = 744) advanced FMR matched (1:2) on infarct size/distribution, patients with advanced FMR had increased adverse mitral apparatus remodeling, paralleled by greater ischemic/dysfunctional subpapillary myocardium (p 0.001). Although posteromedial papillary ischemia was more common with advanced FMR (p = 0.006), subpapillary ischemia with dysfunction remained associated (p 0.001), adjusting for posteromedial papillary ischemia (p = 0.074). During follow-up (median 5.1 years), 1,473 deaths occurred in the overall cohort; advanced FMR conferred increased mortality risk (hazard ratio: 1.52; 95% confidence interval: 1.25 to 1.86; p 0.001) controlling for left ventricular ejection fraction, infarction, and ischemia.Ischemic and dysfunctional subpapillary myocardium provides a substrate for FMR, which predicts mortality independent of key mechanistic substrates.

This research was funded by Junta de Andalucia Grupo de Investigacion CTS113, Spain., The main issue in the prevention of myocardial infarction (MI) is to reduce risk factors. Periodontal disease is related to cardiovascular disease and both share risk factors. The purpose of this study is to investigate whether periodontitis can be considered a risk factor for MI and common risk factors in a case–control study and in a prospective follow-up study in patients with MI. The test group (MIG) was made up of 144 males who had MI in the previous 48 h. The control group (CG) was composed of 138 males without MI. Both groups were subdivided according to the presence or absence of stage III and IV of periodontitis. General data; Mediterranean diet and physical activity screening; periodontal data; and biochemical, microbiological and cardiological parameters were recorded. ANOVA, Mann–Whitney U and Kruskal–Wallis statistical tests and binary logistic regression analysis were applied. No differences in anthropometric variables were observed between the four groups. The average weekly exercise hours have a higher value in CG without periodontitis. The number of leukocytes was higher in MIG, the number of monocytes was higher in CG and the number of teeth was lower in MIG with periodontitis. Adherence to the Mediterranean diet was higher in CG. Porphyromonas gingivalis and Tannerella forsythia were higher in CG with periodontitis and in MIG with and without periodontitis. At follow-up, the left ventricular ejection fraction (LVEF) data were better in the non-periodontitis group: 15 patients had Mayor Cardiovascular Adverse Events (MACE), 13 of them had periodontitis and 2 did not show periodontitis. Periodontitis, exercise, diet and smoking are risk factors related to MI. MACE presented in the ‘MI follow-up’ shows periodontitis, weight, exercise hours and dyslipidemia as risk factors. LVEF follow-up values are preserved in patients without periodontitis. Our data suggest that periodontitis can be considered a risk factor for MI and MACE in the studied population., Junta de Andalucia

Left ventricular (LV) ischemia has been variably associated with functional mitral regurgitation (FMR). Determinants of FMR in patients with ischemia are poorly understood.This study sought to test whether contractile mechanics in ischemic myocardium underlying the mitral valve have an impact on likelihood of FMR.Vasodilator stress perfusion cardiac magnetic resonance was performed in patients with coronary artery disease (CAD) at multiple centers. FMR severity was confirmed quantitatively via core lab analysis. To test relationship of contractile mechanics with ischemic FMR, regional wall motion and strain were assessed in patients with inducible ischemia and minimal (≤5% LV myocardium, nontransmural) infarction.A total of 2,647 patients with CAD were studied; 34% had FMR (7% moderate or greater). FMR severity increased with presence (P 0.001) and extent (P = 0.01) of subpapillary ischemia: patients with moderate or greater FMR had more subpapillary ischemia (odds ratio [OR]: 1.13 per 10% LV; 95% CI: 1.05-1.21; P = 0.001) independent of ischemia in remote regions (P = NS); moderate or greater FMR prevalence increased stepwise with extent of ischemia and infarction in subpapillary myocardium (P 0.001); stronger associations between FMR and infarction paralleled greater wall motion scores in infarct-affected territories. Among patients with inducible ischemia and minimal infarction (n = 532), wall motion and radial strain analysis showed impaired subpapillary contractile mechanics to associate with moderate or greater FMR (P 0.05) independent of remote regions (P = NS). Conversely, subpapillary ischemia without contractile dysfunction did not augment FMR likelihood. Mitral and interpapillary dimensions increased with subpapillary radial strain impairment; each remodeling parameter associated with impaired subpapillary strain (P 0.05) independent of remote strain (P = NS). Subpapillary radial strain (OR: 1.13 per 5% [95% CI: 1.02-1.25]; P = 0.02) and mitral tenting area (OR: 1.05 per 10 mmAmong patients with CAD and ischemia, FMR severity and adverse mitral apparatus remodeling increase in proportion to contractile dysfunction underlying the mitral valve.

There are several approaches widely used in the localization of the responsible artery in inferior myocardial infarction. However, the existing papers show differences in the point where the ST segment is measured. The purpose of our investigation is to analyse the influence of the point at which elevation of the ST segment is measured on the results of these algorithms.We analysed the 12‑lead electrocardiograms of 90 consecutive patients with inferior myocardial infarction. The ST segment elevation or depression was measured at the J-point and at 80 ms, and three algorithms were applied to predict the culprit artery with both measurements. Sensitivity, specificity, the area under the curve, and the kappa index of agreement were analysed to compare each algorithm at the J-point and at 80 ms.The area under the curve was better at the J-point than at 80 ms in two algorithms (0.696 vs. 0.635, p 0.043, and 0.754 vs. 0.661, p 0.045) and did not change in one. Agreement between the J-point and 80 ms was suboptimal in all three algorithms (0.71, 0.65, and 0.58).The result of different algorithms to detect the culprit artery in inferior STEMI patients can change significantly depending on the point where ST elevation or depression is measured.

Background Seemingly conflicting findings exist regarding the prognostic impact of totally occluded infarct-related arteries (oIRA) in non-ST elevation acute coronary syndromes (NSTE-ACS). Methods Retrospective analysis of prospective multicenter registry data comprising a single-center NSTE-ACS cohort, aimed at assessing the impact of occluded (TIMI flow 0/1) versus patent culprit vessels (pIRA, TIMI flow 2/3) on the composite endpoint of all-cause death and cardiogenic shock events at 30 days. Results Of 568 patients, 183 (32.5%) had oIRA. Male sex, refractory angina, ECG suggestive of multivessel or left main disease, and larger infarct sizes with inferior/posterolateral wall involvement, were identified as highly specific markers of oIRA. Successful culprit-lesion revascularization occurred more frequently in patent than in oIRA (90% vs. 96%; P = 0.013). Conversely, patients with oIRA more frequently achieved successful revascularization of concurrent non-IRAs including chronic total occlusions than did those with pIRA (28% vs. 3%; P = 0.0005). Multivariate analysis revealed neutral effects of oIRA on outcomes and identified incomplete revascularization as a powerful predictor of mortality. Moderation analysis revealed a significant interaction between completeness of revascularization and IRA patency, whereby among the incompletely revascularized patients, those with oIRA enjoyed a significant survival advantage over their counterparts with pIRA (11.8% vs. 28%, adjusted OR 0.34; 95% CI 0.10–0.73; P interaction = 0.012). Conclusions Approximately one third of NSTE-ACS patients in this cohort had oIRA. However, compared with pIRA, the occurrence of oIRA did not portend poor outcomes, likely resulting from the higher rate of incomplete revascularization and increased risk of subsequent mortality in patients with pIRA. These exploratory findings warrant further investigation.