1,721,163 research outputs found
Prevalence of echocardiographic left-atrial enlargement in hypertension : a systematic review of recent clinical studies
No full textBackground Left atrial enlargement (LAE) is a marker of hypertensive heart disease associated with increased cardiovascular risk. We reviewed recent literature about the prevalence of LAE, as assessed by echocardiography, to update our information about the clinical relevance of this cardiac phenotype in human hypertension. Methods We performed a search of MEDLINE using the key words "left atrial enlargement," "left atrial dilatation," "left atrial size," "hypertension," "echocardiography, " and "atrial fibrillation" to identify relevant papers. We considered full articles published in English from January 1, 2000 to July 1, 2012 reporting studies involving adult individuals. Results We analyzed a total of 15 studies, including 10,141 untreated and treated subjects. LAE was defined according to 11 different criteria (4 studies applied two or three criteria), and its prevalence consistently varied among studies, from 16.0-83.0%, with a prevalence in the pooled population of 32%. A gender-based analysis of 9 studies (8,588 patients) showed the prevalence of LAE as being similar in women and men (OR, 1.23; 95% CI, 0.83-1.83; P = 0.30). Data provided by 10 studies (n = 9,354 patients) showed the prevalence of left-ventricular hypertrophy as being significantly higher in patients with LAE (68.2%) than in their counterparts without LAE (41.8%) (OR, 2.97; 95% CI, 2.68-3.29; P < 0.01).CONCLUSIONSOur analysis shows that LAE is present in a relevant fraction of the hypertensive population. Because LAE is an independent predictor of cardiovascular events, the accurate detection of this phenotype may improve the evaluation of risk in hypertensive patients
Targeting hypertensive myocardial fibrosis
No full textIn normal myocardium, myocytes represent only one-third of all cells, with the remaining two-thirds including fibroblasts and small cellular populations. While several weeks post partum the myocyte count stops increasing, the connective tissue cell count does not. In the early phases of arterial hypertension, adaptive left ventricular (LV) hypertrophy (LVH) is characterised by the growth of cardiac myocytes, which may or may not be accompanied by other alterations in tissue structure. In hypertensive heart disease, however, complex changes in myocardial composition occur, with a disproportionate involvement of noncardiomyocyte cells accounting for a pathological remodelling of tissue structure (pathological hypertrophy). Myocardial fibrosis is the result of both haemodynamic and nonhaemodynamic factors playing a synergistic role and reflects the loss of the physiological reciprocal regulation between stimulatory and inhibitory factors acting on the turnover of fibrillar collagen. Cardiac biopsy is the gold standard for assessing myocardial fibrosis; in the last decades different non-invasive approaches have been developed and validated to detect and follow-up cardiac fibrosis, including biochemical markers of collagen synthesis and degradation, cardiac hormones and ultrasonographic procedures. Due to the clinical implications of myocardial fibrosis and pathological LVH, it is of great interest to ascertain the effect of antihypertensive agents on cardiac structure: the optimal treatment of hypertensive patients should target a parallel decrease in cardiac mass and fibrosis. Preliminary evidence suggests that not all antihypertensive drugs affect fibrosis to the same extent: angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers (ARBs) appear particularly effective, in contrast to β-blockers and diuretics. Finally, the impact of fibrosis and its regression on subsequent cardiovascular events when compared with LV mass and its reduction remain to be investigated
Evaluation of the 24 hours sympatho-vagal balance by the phase-space distribution of arterial blood pressure monitoring (ABPM) values
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