Hypertensive Dilated Cardiomyopathy Research Articles

Epidemiology and Management of Heart Failure in the Medicine Department of Tombouctou Hospital

Introduction: Heart failure is a complex syndrome and very frequently observed and secondary to the outcome of many advanced heart diseases. It is made up of a set of symptoms that reflect the tissue and visceral consequences of heart failure. The objective was to determine the hospital prevalence and to describe the management of heart failure in the medical department of Tombouctou hospital in Mali. Methods: This is a descriptive cross-sectional study with retrospective data collection, carried out over 24 months and involving the analysis of 266 records of patients hospitalized for heart failure. Results: The frequency of heart failure was 17.6% with a female predominance. The average age was 48 years with extremes of 16 and 90 years. Cardiovascular risk factors were dominated by high blood pressure with 38%. Global heart failure was the mode of discovery in 72.2% of cases. The etiologies were dominated by hypertensive dilated cardiomyopathy in 36.8% and peripartum cardiomyopathy in 32% of cases. The majority of our patients benefited from diuretic treatment, i.e. 95.9% frequency; with a favorable evolution in 96.2% of cases. We recorded 10 deaths, i.e. a lethality of 3.7%. We report some difficulties encountered during our security study because Tombouctou is a war zone and the lack of a technical platform for biology such as (BNP or NT-proBNP). Conclusion: Heart failure is a real public health problem. Its prevalence is increasing due to the aging of the population and especially the poor management of arterial hypertension in our context.

Neuro-Psychological Pattern in Patients Suffering from Primitive Dilated Cardiomyopathy with Impairment in Executive Function.

According to the American Heart Association (AHA), primitive dilated cardiomyopathy (PDCM) is a "progressive dilation of the left or both ventricles and a depressed contractility in the absence of abnormal load conditions". It evolves in progressive heart-failure. The term "cardiogenic dementia" expresses the intimate connection between heart diseases and cognitive functions. The association between PDCM and the neuropsychological functions is unclear: the main pathophysiological hypotheses are cerebral hypoperfusion and cardiogenic emboli. The aim of this study is to evaluate the impact that the PDCM has on neuropsychological decline and to detect early echocardiographic markers of cognitive impairment. We enrolled 235 patients: 168 suffering from PDCM as sample group and 67 suffering from hypertensive dilated cardiomyopathy (HTCM) as control group. They underwent a cardiology examination and a neuropsychological assessment. A p<0.05 was considered significant. The two groups showed no differences in risk factors, demographic and cardiovascular parameters (except for dimensions of aortic root, left atrium and ventricle which appeared greater in PDCM and left ventricle ejection fraction that appeared lower in PDCM). Among administered neuropsychological tests, only the Stroop Test (which explores executive and attentive functions) appeared significantly lower in PDCM (p = 0.029). Moreover left ventricle end-diastolic diameter was inversely related to the Stroop Test Score (r= -0.32). PDCM doesn't appear to be at the basis of a generalized cognitive and neuropsychological decline. Only the executive functions seem impaired in PDCM. Left ventricle dilation seems to be associated to attentive and executive functions decline.

Postconditioning Protects Against Reperfusion Injury in Hypertensive Dilated Cardiomyopathy by Activating MEK/ERK1/2 Signaling

BackgroundPostconditioning (PostC) cardioprotection has been related to up-regulation of survival kinases; however, the efficacy of PostC and the role of ERK1/2 (extracellular signal-regulated kinase 1/2) remain to be substantiated in hypertension states that may produce “pathologic remodeling.” Therefore, in this work we compared PostC effect and assessed the role of ERK1/2 activation in a model of hypertensive dilated cardiomyopathy (DCM), versus normal (Sham) and compensated hypertrophy (CH) models. Methods and ResultsRats were subjected to angiotensin II administration until development of cardiovascular diseases. Then, isolated hearts underwent ischemia followed by PostC and reperfusion. PostC maintained the double product in all groups. PostC reduced infarct size from 36.16 ± 3% to 9.8% ± 2.2 in Sham, from 37.5 ± 2.4% to 12 ± 3% in CH, and from 40 ± 2.4% to 11.55 ± 3% in DCM. Inhibition of the mitogen-activated protein kinase kinase (MEK)/ERK1/2 pathway had different effects on PostC-conferred cardioprotection in the evaluated groups. Interestingly, although phosphatidylinositol-3-kinase activation was negligible in PostC DCM hearts, we observed Akt activation. ConclusionsPostC confers cardioprotection through alternative survival pathways in normal and CH hearts, and cardiac function recovery in DCM relies mainly on MEK/ERK1/2 cascade. Down-regulation of phosphatidylinositide 3-kinase does not affect the cardioprotective response in DCM, because MEK/ERK1/2 cascade may convey direct Akt activation, strengthening downstream signaling.

Coronary reserve impairment prevents the improvement of left ventricular dysfunction and adversely affects the long-term outcome of patients with hypertensive dilated cardiomyopathy

In hypertension, left ventricular (LV) hypertrophy develops as an adaptive mechanism to compensate for increased afterload and thus preserve systolic function. Associated structural changes such as microvascular disease might potentially interfere with this mechanism, producing pathological hypertrophy. A poorer outcome is expected to occur when LV function is put in jeopardy by impaired coronary reserve. The aim of this study was to evaluate the role of coronary reserve in the long-term outcome of patients with hypertensive dilated cardiomyopathy. Between 1996 and 2000, 45 patients, 30 of them male, with 52 ± 11 years and LV fractional shortening <30% were enrolled and followed until 2006. Coronary flow velocity reserve was assessed by transesophageal Doppler of the left anterior descending coronary artery. Sixteen patients showed ≥10% improvement in LV fractional shortening after 17 ± 6 months. Coronary reserve was the only variable independently related to this improvement. Total mortality was 38% in 10 years. The Cox model identified coronary reserve (hazard ratio = 0.814; 95% CI = 0.72–0.92), LV mass, low diastolic blood pressure, and male gender as independent predictors of mortality. In hypertensive dilated cardiomyopathy, coronary reserve impairment adversely affects survival, possibly by interfering with the improvement of LV dysfunction.

Interaction of BMP10 with Tcap may modulate the course of hypertensive cardiac hypertrophy

Elevated wall stress by hypertension induces an adaptive myocardial hypertrophy via releasing prohypertrophic hormones such as angiotensin II. In this study, we investigated the involvement of bone morphogenetic protein-10 (BMP10) in hypertension-induced cardiac hypertrophy. Expression of BMP10 was increased in the hypertrophied ventricles from hypertensive rats. BMP10 localized on cell surface and at stretch-sensing Z disc of cardiomyocytes, where BMP10 interacted with a protein called titin-cap (Tcap). A rare variant of the human BMP10 gene, Thr326Ile, was found to be associated with hypertensive dilated cardiomyopathy. The variant BMP10 demonstrated decreased binding to Tcap and increased extracellular secretion. Conditioned medium from cells transfected with wild-type or variant BMP10 induced hypertrophy in rat neonatal cardiomyocytes, except that medium from variant BMP10-carrying cells showed an enhanced effect reflecting the increased secretion. These observations suggested that hypertension induced expression of prohypertrophic BMP10, and the hypertrophic effect of BMP10 was modulated, at least in part, by its binding to Tcap at the Z disc.