Subject(s)
Acidosis, Lactic/drug therapy , Beriberi/drug therapy , Recovery of Function/drug effects , Shock, Cardiogenic/drug therapy , Thiamine/administration & dosage , Vitamin B Complex/administration & dosage , Acidosis, Lactic/diagnosis , Acidosis, Lactic/physiopathology , Adolescent , Beriberi/diagnosis , Beriberi/physiopathology , Electrocardiography/drug effects , Female , Humans , Recovery of Function/physiology , Shock, Cardiogenic/diagnosis , Shock, Cardiogenic/physiopathologyABSTRACT
AIM: Catecholamine excess along with an exaggerated sympathetic stimulation appears to play a major role in the pathophysiological mechanism of tako-tsubo cardiomyopathy (TTC), which mimics acute ST-elevation myocardial infarction (STEMI). The aim of the present study was to investigate differences in the distribution of allelic variants of ß1- and ß2-adrenoceptors between TTC and anterior STEMI patients compared to normal subjects. METHODS AND RESULTS: ß1- and/or ß2-adrenoceptor polymorphisms in 97 patients with TTC (92 females, 96%; mean age 66.8±11.6years; range 35 to 87years) were compared with 81 patients with anterior STEMI (77 females, 95%; mean age 72.5±12.8years; range 32 to 96years) and 101 controls (95 females, 94%; mean age 62.3±10.4years; range 44 to 92years). Differences in genotype frequencies were assessed using the Pearson χ(2) test. ß1-Adrenoceptor (Gly389Arg) and ß2-adrenoceptor (Arg16Gly and Gln27Glu) genotype frequencies were significantly different among groups (p<0.001, p=0.024, p=0.008, respectively). However, differences did not achieve statistical significance when TTC and anterior STEMI patients were compared by post-hoc analysis. The cardiovascular risk factor profile was worse in anterior STEMI patients, who more often had a history of systemic arterial hypertension, diabetes and coronary artery disease. CONCLUSIONS: In a large TTC cohort compared with anterior STEMI patients, ß-adrenoceptor polymorphisms were similar. However, the cardiovascular risk factor profile was different between the two groups. ß-Adrenoceptor polymorphisms in TTC patients differed from normal subjects.
Subject(s)
Cardiomyopathies/genetics , Cardiovascular Diseases/genetics , Myocardial Infarction/genetics , Polymorphism, Single Nucleotide/genetics , Receptors, Adrenergic, beta-1/genetics , Receptors, Adrenergic, beta-2/genetics , Takotsubo Cardiomyopathy/genetics , Aged , Aged, 80 and over , Cardiomyopathies/pathology , Cardiovascular Diseases/pathology , Coronary Artery Disease/complications , Coronary Artery Disease/etiology , Diagnosis, Differential , Female , Genotype , Humans , Male , Middle Aged , Myocardial Infarction/pathology , Risk Factors , Takotsubo Cardiomyopathy/pathology , Takotsubo Cardiomyopathy/physiopathology , White People/geneticsABSTRACT
Effective treatment of high blood pressure levels represents a key strategy for reducing global cardiovascular risk. Other factors, beyond blood pressure control, however, appear to be of potential relevance in reducing the risk related to hypertension. Recent clinical trials have demonstrated that those pharmacological agents that counteract the renin-angiotensin system may confer additional clinical benefits across the spectrum of cardiovascular disease, beyond their blood pressure-lowering properties. These studies are largely based on the use of an antihypertensive strategy, based on the association between angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (ARBs) and low-dose thiazide diuretics or calcium channel blockers. Over the last few decades, clinical trials have also tested the potential effects of combination therapy based on the association between angiotensin-converting enzyme inhibitors or ARBs and other renin-angiotensin system-blocking agents, including mineralocorticoid receptor antagonists and, more recently, renin inhibitors. This review highlights the evidence derived from recent clinical trials, supporting a role for pharmacological strategies based on ARBs in primary and secondary prevention of cardiovascular and renal disease.