Impairment Of Left Ventricle Function Research Articles

Left Main Total Chronic Occlusion in a Patient with Colorectal Cancer: A Case Report of a Rare and Severe Localization of Coronary Artery Disease

The aim of this case report is to draw attention at the potential severity of presentation of these associated pathologies. Prevention through early screening of colorectal cancer in patients with coronary artery disease and vice versa is the guarantee of a better management of the two pathologies. Cardiovascular disease and cancer are the two leading causes of death worldwide. Emerging evidence suggests associations between cardiovascular disease and several cancers, including colorectal cancer. Many cases have reported severe coronary artery disease (CAD) in association with colorectal cancer including triple vessel disease. To the best of our knowledge this is the first case reporting a total occlusion of the left main coronary artery in such patients.
 We report the case of a 52 years old woman presented to our cath lab for severe angina (Class III of the Canadian classification) and impairment of left ventricle function. Six months before the patient was diagnosed with a metastatic colorectal cancer. Coronary angiography showed absence of anterograde opacification of the left coronary system. Selective right coronary artery angiography showed a retrograde filling of the left coronary system by collaterals issued from proximal and distal dominant right coronary artery.
 Several studies have reported the association between colorectal neoplasm and CAD but Isolated left main coronary artery disease is extremely uncommon. Patients with left main coronary artery disease have always a grim prognosis and without prompt revascularization 60% will die after 5 years while survivors live with severe angina; heart failure or both.

Paramètres cliniques et échocardiographiques associés à l'altération du strain longitudinal global dans l'insuffisance mitrale secondaire

IntroductionLeft ventricular systolic function may be overestimated in patients with secondary mitral regurgitation when using left ventricle ejection fraction. The Global longitudinal strain is a measure less dependent on left ventricle load. However, the clinical and echocardiographic parameters associated with the alteration of Global longitudinal strain in secondary mitral regurgitation have not been evaluated. Material and methodsA total of 96 patients (mean age 62.3 ± 12.1 years, 59.3% male) with secondary mitral regurgitation and low left ventricle ejection fraction < 50% were included. The study population was subdivided according to the Global longitudinal strain value with which an increased risk of all-cause mortality was associated (Global longitudinal strain < 7.0%, left ventricle systolic function impaired compared to Global longitudinal strain ≥ 7.0%, in absolute value). The clinical and echocardiographic endpoints are analysed in both groups of patients. ResultsThe strong and clear correlation between Global longitudinal strain (mean ± standard deviation: 7,2 ± 2,7) and parameters of systolic function (left ventricle ejection fraction mean ± standard deviation: 32,4 ± 8,0%) and contractility (dp/dt mean ± standard deviation: 682,5 ± 204,7 mmHg/s). the mean of left ventricle ejection fraction = 26.4 ± 5.3% in the Global longitudinal strain < 7 group, and the bivariate study using the 30% threshold shows that the Global longitudinal strain < 7 group presents a more altered left ventricle ejection fraction with odds ratio = 12, 5 (CI: 4.7–33.0) p < 0.001. In multivariate analysis of ultrasound parameters and linear regression shows a significant correlation between Global longitudinal strain and left ventricle ejection fraction (p < 0.001). The dp/dt analysis found a mean of 509.3 ± 99.1 mmHg/s in the Global longitudinal strain < 7 group and of 822.9 ± 154.1 in the Global longitudinal strain ≥ 7 group with significant difference (p < 0.001). In bivariate and multivariate analysis, the alteration of Global longitudinal strain is associated with a significantly lower dp / dt p < 0.001. ConclusionA Global longitudinal strain < 7 (in absolute value) reflects a severe impairment of left ventricle function. In addition, several parameters were associated with this severe alteration of the Global longitudinal strain, namely a lower left ventricle ejection fraction, a lower dp/dt and more severe symptoms permitting to characterized this group of patients in addition to an integration in a multiparametric evaluation of the secondary mitral regurgitation.

Epoxyeicosatrienoic Acid-Based Therapy Attenuates the Progression of Postischemic Heart Failure in Normotensive Sprague-Dawley but Not in Hypertensive Ren-2 Transgenic Rats.

Epoxyeicosatrienoic acids (EETs) and their analogs have been identified as potent antihypertensive compounds with cardio- and renoprotective actions. Here, we examined the effect of EET-A, an orally active EET analog, and c-AUCB, an inhibitor of the EETs degrading enzyme soluble epoxide hydrolase, on the progression of post-myocardial infarction (MI) heart failure (HF) in normotensive Hannover Sprague-Dawley (HanSD) and in heterozygous Ren-2 transgenic rats (TGR) with angiotensin II-dependent hypertension. Adult male rats (12 weeks old) were subjected to 60-min left anterior descending (LAD) coronary artery occlusion or sham (non-MI) operation. Animals were treated with EET-A and c-AUCB (10 and 1 mg/kg/day, respectively) in drinking water, given alone or combined for 5 weeks starting 24 h after MI induction. Left ventricle (LV) function and geometry were assessed by echocardiography before MI and during the progression of HF. At the end of the study, LV function was determined by catheterization and tissue samples were collected. Ischemic mortality due to the incidence of sustained ventricular fibrillation was significantly higher in TGR than in HanSD rats (35.4 and 17.7%, respectively). MI-induced HF markedly increased LV end-diastolic pressure (Ped) and reduced fractional shortening (FS) and the peak rate of pressure development [+(dP/dt)max] in untreated HanSD compared to sham (non-MI) group [Ped: 30.5 ± 3.3 vs. 9.7 ± 1.3 mmHg; FS: 11.1 ± 1.0 vs. 40.8 ± 0.5%; +(dP/dt)max: 3890 ± 291 vs. 5947 ± 309 mmHg/s]. EET-A and c-AUCB, given alone, tended to improve LV function parameters in HanSD rats. Their combination amplified the cardioprotective effect of single therapy and reached significant differences compared to untreated HanSD controls [Ped: 19.4 ± 2.2 mmHg; FS: 14.9 ± 1.0%; +(dP/dt)max: 5278 ± 255 mmHg/s]. In TGR, MI resulted in the impairment of LV function like HanSD rats. All treatments reduced the increased level of albuminuria in TGR compared to untreated MI group, but neither single nor combined EET-based therapy improved LV function. Our results indicate that EET-based therapy attenuates the progression of post-MI HF in HanSD, but not in TGR, even though they exhibited renoprotective action in TGR hypertensive rats.

Left Ventricle Function During Therapeutic Hypothermia with Beta1-Adrenergic Receptor Blockade.

Therapeutic hypothermia is an established treatment in patients resuscitated from cardiac arrest. It is usually well-tolerated circulatory, but hypothermia negatively effects myocardial contraction and relaxation velocities and increases diastolic filling restrictions. A significant proportion of resuscitated patients are treated with long-acting beta-receptor blocking agents' prearrest, but the combined effects of hypothermia and beta-blockade on left ventricle (LV) function are not previously investigated. We hypothesized that beta1-adrenergic receptor blockade (esmolol infusion) exacerbates the negative effects of hypothermia on active myocardial motions, affecting both systolic and diastolic LV function. A pig (n = 10) study was performed to evaluate the myocardial effects of esmolol during hypothermia (33°C) and during normothermia, at spontaneous and pacing-increased heart rates (HRs). LV function was assessed by a LV pressure transducer, an epicardial ultrasonic transducer (wall thickness, wall thickening/thinning velocity) and an aortic ultrasonic flow-probe (stroke volume, cardiac output). The data were compared using a paired two-tailed Students t-test, and also analyzed using a linear mixed model to handle dependencies introduced by repeated measurements within each subject. The significance level was p ≤ 0.05. The effects of hypothermia and beta blockade were distinct and additive. Hypothermia reduced myocardial motion velocities and increased diastolic filling restrictions, but end-systolic wall thickness increased, and stroke volume and dP/dtmax (pumping function) were maintained. In contrast, esmolol predominantly affected systolic pumping function, by a negative inotropic effect. In combination, hypothermia and esmolol reduced myocardial velocities in systole and diastole by ∼40%, compared with normothermia without esmolol, inducing in combination both systolic and diastolic LV function impairment. The cardiac dysfunction deteriorated at increased HRs during hypothermia. Beta1-adrenergic receptor blockade (esmolol) exacerbates the negative effects of hypothermia on active myocardial contraction and relaxation. The combination of hypothermia with beta-blockade induces both systolic and diastolic LV function impairment.

Evaluation of left ventricular strain in patients with dilated cardiomyopathy.

ObjectiveDilated cardiomyopathy (DCM) can cause structural and functional changes in the left ventricle (LV). In this study, we evaluated whether cardiac magnetic resonance tissue-tracking (MR-TT) can be applied to the detection of LV abnormalities in patients with DCM.MethodsWe used MR-TT to analyze the global peak radial strain (GPRS), global peak circumferential strain (GPCS), and global peak longitudinal strain (GPLS) in every segment of the LV in 23 patients with DCM and 25 controls. The LV ejection fraction was also measured as a function indicator.ResultsCompared with the controls, the GPRS, GPCS, and GPLS were significantly reduced in patients with DCM, indicating global LV function impairment in all directions. We also identified a significant linear correlation between the GPRS, GPCS, and GPLS and the LV ejection fraction, indicating that LV function relies on coordinated wall motion from all directions. Moreover, we found that patients with DCM had a significantly reduced magnitude of the PRS, PCS, and PLS in most segments at different levels, indicating impaired myocardial function in most LV regions.ConclusionsOur results demonstrate that LV myocardial strain in patients with DCM can be sensitively detected by MR-TT (not only the global LV function changes but also the segmental strain), which can help to identify the injured segment at an early stage and guide clinical treatment.

Assessment of left ventricle function in patients with symptomatic and asymptomatic aortic stenosis by 2-dimensional speckle-tracking imaging

SummaryBackgroundGlobal longitudinal peak strain (GLPS) quantifies left ventricle (LV) long-axis contractility. Early detection of LV systolic dysfunction is pivotal in diagnosis and treatment of patients with aortic stenosis (AS). This study was performed to assess LV longitudinal systolic function by GLPS derived from 2-dimensional speckle tracking imaging (2D-STI) in AS patients in comparison to standard echocardiographic parameters.Material/MethodsLaboratory tests, standard echocardiography, tissue Doppler imaging (TDI) and 2D-STI examinations with GLPS calculation were performed in 49 consecutive patients with moderate to severe AS with LV ejection fraction ≥50% and 18 controls.ResultsWhile LVEF do not differentiate AS patients from controls, GLPS was significantly decreased in the AS group (−15.30±3.25% vs. −19.60±2.46% in controls, p<0.001). GLPS was significantly reduced in symptomatic AS patients as compared to the asymptomatic AS group [−15.5 (11.8–16.8) vs. −17.5 (14.7–18.9)%, p=0.02].ConclusionsIn aortic stenosis patients, despite normal left ventricle ejection fraction, long-axis left ventricular function is impaired, which manifests in global longitudinal peak strain reduction. GLPS reveals that LV function impairment is more pronounced in symptomatic as compared to asymptomatic AS patients. Further studies are needed to determine the prognostic significance of early LV function impairment in aortic stenosis patients showed by GLPS.

Myocardial Function After Gut Ischemia/Reperfusion: Does NFκB Play a Role?

Mesenteric ischemia/reperfusion (I/R) is a common problem in critically ill patients and is frequently associated with myocardial dysfunction. Several potential mechanisms have been proposed to be involved in the myocardial dysfunction associated with mesenteric I/R, including nuclear factor kappa B (NF kappaB)-mediated tumor necrosis factor alpha (TNF-alpha) release leading to cardiodepression. Thus, we sought to investigate the effect of NF kappaB inhibition on mesenteric I/R-associated myocardial dysfunction in a large animal model (dog). A total of 21 mongrel dogs were anesthetized and mechanically ventilated. Animals were instrumented with a Swan-Ganz Catheter, left ventricle (LV) pressure manometer, and ultrasonic crystals. Mesenteric I/R consisted of 60 min of ischemia followed by 180 min of reperfusion. Seven animals received pyrrolidine dithiocarbamate (PDTC, 100 mg/kg) prior to mesenteric I/R (I/R PDTC). Another group of animals (n = 7) without mesenteric ischemia received PDTC following baseline measurements and served as control for the effect of PDTC alone (PDTC). Preload recruitable stroke work, +/-dp/dt(max), isovolumic relaxation (tau), and cardiac output were measured. Myocardial tissue was analyzed for NF kappaB activity, TNF-alpha production, and myocardial apoptosis. Mesenteric I/R impaired both LV systolic and diastolic function. Administration of PDTC worsened LV function impairment following I/R. In addition, PDTC resulted in decreased LV function even without mesenteric I/R. NF kappaB, TNF-alpha, and myocardial apoptosis were not different among the groups. Mesenteric I/R affects LV function independent of NF kappaB and TNF-alpha pathways. PDTC acts as a cardiac depressant through a thus far unknown mechanism. Therefore, evaluation of cardiac and hemodynamic function in experimental setups using PDTC has to be carefully interpreted.

790 Relationship between HRT and HRV in patients with postinfarction impairment of left ventricle function and different types of ventricular arrhythmias

790 Relationship between HRT and HRV in patients with postinfarction impairment of left ventricle function and different types of ventricular arrhythmias

Is there progress in the autopsy diagnosis of sudden unexpected death in adults?

Sudden death is now currently described as natural unexpected death occurring within 1 h of new symptoms. Most studies on the subject focused on cardiac causes of death because most of the cases are related to cardiovascular disease, especially coronary artery disease. The incidence of sudden death varies largely as a function of coronary heart disease prevalence and is underestimated. Although cardiac causes are the leading cause of sudden death, the exact incidence of the other causes is not well established because in some countries, many sudden deaths are not autopsied. Many risk factors of sudden cardiac death are identified: age, gender, heredity factors such as malignant mutations, left ventricular hypertrophy and left ventricle function impairment. The role of the police surgeon in the investigation of sudden death is very important. This investigation requires the interrogation of witnesses and of the family members of the deceased. The interrogation of physicians of the rescue team who attempted resuscitation is also useful. Recent symptoms before death and past medical history must be searched. Other sudden deaths in the family must be noted. The distinction between sudden death at rest and during effort is very important because some lethal arrhythmia are triggered by catecholamines during stressful activity. The type of drugs taken by the deceased may indicate a particular disease linked with sudden death. Sudden death in the young always requires systematic forensic autopsy performed by at least one forensic pathologist. According to recent autopsy studies, coronary artery disease is still the major cause of death in people aged more than 35 years. Cardiomyopathies are more frequently encountered in people aged less than 35 years. The most frequent cardiomyopathy revealed by sudden death is now arrhythmogenic right ventricular cardiomyopathy also known simply as right ventricular cardiomyopathy (RVC). The postmortem diagnosis of cardiomyopathies is very important because the family of the deceased will need counseling and the first-degree relatives may undergo a possible screening to prevent other sudden deaths. In each case of sudden death, one important duty of the forensic pathologist is to inform the family of all autopsy results within 1 month after the autopsy. Most of the recent progress in autopsy diagnosis of sudden unexpected death in the adults comes from molecular biology, especially in case of sudden death without significant morphological anomalies. Searching mutations linked with functional cardiac pathology such as long-QT syndrome, Brugada syndrome or idiopathic ventricular fibrillation is now the best way in order to explain such sudden death. Moreover, new syndromes have been described by cardiologists, such as short-QT syndrome and revealed in some cases by a sudden death. Molecular biology is now needed when limits of morphological diagnosis have been reached.

Coenzyme Q10 and key enzyme activities in papillary muscle related to left ventricle function in mitral valve disease.

Coenzyme Q10 (CoQ10) was studied in papillary muscle from 18 patients (52-67 years, 2 females) subjected to open heart surgery due to mitral valve disease. In addition the enzyme activities of lactate dehydrogenase (LD) with its five isozymes, citrate synthase (CS) and mitochondrial CK (CK-MIT) were determined. Myocardial function was assessed by means of left ventricle (LV) angiography. CoQ10 averaged 0.39 (range 0.26-0.59) micrograms x mg-1 dw. On an individual basis CoQ10 was related to CS activity although not as closely as CK-MIT (r = 0.45, p less than 0.05 versus r = 0.86, p less than 0.001). The ratio (CoQ10) x (CS activity)-1 was calculated to represent mitochondrial quality. The level of LD3 fraction increase was used to mark for the degree of metabolic stress in the heart. LD3 fraction was negatively related to the quality index (r = -0.71, p less than 0.001). Thus, those with a low CoQ10 per unit of CS activity had also a high LD3 isozyme fraction. In a subset of 12 patients with isolated mitral regurgitation due to myxomatous valve degeneration, CoQ10 and the ratio CoQ10 over CS decreased with the degree of LV function impairment (r = -0.58, p less than 0.05 and r = -0.68, p less than 0.05, respectively). The quality index takes into account not only enzyme activity but also the potential for control of free oxygen radicals.