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BACKGROUND
Patients undergoing aortic valve replacement for critical aortic stenosis often have significant left ventricular hypertrophy. Left ventricular hypertrophy has been identified as an independent predictor of poor outcome after aortic valve replacement as a result of a combination of
Peri-operative arrhythmia is one of the major complications in anaesthesia for valve replacement surgery in patients with aortic stenosis. In this retrospective study, 58 patients with sinus rhythm were investigated from induction of anaesthesia until arrival at the recovery room by close
A decrease of the transient outward potassium current (Ito) has been observed in cardiac hypertrophy and contributes to the altered shape of the action potential (AP) of hypertrophied ventricular myocytes. Since the shape and duration of the ventricular AP are important determinants of the Ca2+
BACKGROUND
Although family history can be an important risk factor for cardiovascular disease, relatively little is known about the nature of specific genetic risk factors. One approach to this problem is to identify and characterize genes responsible for inherited disorders in the hope that this
With the increasing age of patients and the progression of degenerative pathologies, the management of aortic stenosis (AS) with coronary artery disease is becoming more frequent. Reported results of combined valve and coronary surgery are equivocal especially with respect to the increased risk
Patients with left ventricular (LV) hypertrophy may suffer ischemia-reperfusion injuries at the time of cardiac surgery with impairment in left ventricular function. Using transesophageal echocardiography (TEE), we evaluated the impact of glucose-insulin potassium (GIK) on LV 18 patients with valvular aortic stenosis were given an i.v. glucose tolerance test and an i.v. insulin tolerance test before and 4-36 months after valve replacement. Insulin and C-peptide response to the glucose challenge was smaller preoperatively whereas the glucose response was the same pre- and
Myocardial oxygen consumption and blood flow distribution were examined in severely hypertrophied canine hearts in the empty-beating, fibrillating, and pharmacologically arrested states. Hypertrophy was produced using a subcoronary valvular aortic stenosis model that mimics the clinical situation of
OBJECTIVE
Ventricular fibrillation (VF) is life-threatening because of its haemodynamic and metabolic effects. The purpose was to examine if VF also has primary effects per se. We therefore investigated the early effects of VF on myocardial blood flow, metabolic characteristics and catecholamine
Cardiac arrest developed in two patients after the administration of oral potassium. Neither patient had renal insufficiency, but both had underlying heart disease. In one patient fatal ventricular fibrillation developed 4 days after he received an aortic valve replacement for aortic stenosis and
Calcific aortic valve disease is associated with increased morbidity and mortality, especially in the elderly. To date, pharmacological therapies have not proven as effective as surgical intervention. Here, we used a hyperlipidemic rabbit model to investigate the potential effects of selective
BACKGROUND
We previously reported that IKAS are heterogeneously upregulated in failing rabbit ventricles and play an important role in arrhythmogenesis. This study goal is to test the hypothesis that subtype 2 of the small-conductance Ca(2+) activated K(+) (SK2) channel and apamin-sensitive K(+)
To evaluate intraoperative changes in myocardial performance during valvular operations, ventricular functional measurements were obtained in 16 patients before and after elective cardiac valvular replacement. Six patients had mitral regurgitation, four had mitral stenosis, and six had calcific
Left ventricular (LV) hypertrophy and myocardial infarction play important roles in the progressive LV dysfunction. We hypothesized that the potassium-channel opener and nitrate-like vasodilator nicorandil prevents the development of LV hypertrophy and preserves myocardial viability. Twenty-four