Background And Purpose: Aortic valve stenosis (AVS) is associated with significant cardiovascular morbidity and mortality. To date, no therapeutic modality has been shown to be effective in retarding AVS progression. We evaluated the effect of angiotensin-converting enzyme inhibition with ramipril on disease progression in a recently developed rabbit model of AVS.
View Article and Find Full Text PDFUnderstanding of the pathophysiology of aortic valve stenosis (AVS) and finding potentially effective treatments are impeded by the lack of suitable AVS animal models. A previous study demonstrated the development of AVS in rabbits with vitamin D(2) and cholesterol supplementation without any hemodynamic changes in the cholesterol supplemented group alone. The current study aimed to determine whether AVS develops in an animal model with vitamin D(2) supplementation alone, and to explore pathophysiological mechanisms underlying this process.
View Article and Find Full Text PDFObjectives: This study sought to compare the influence of changes in systolic interval on the negative inotropic effects of metoprolol, sotalol, and verapamil in patients with ischemic heart disease.
Background: The long-term symptomatic and prognostic effects of antiarrhythmic agents are not easily predicted on the basis of acute hemodynamic actions at rest, but may be unmasked during tachycardia. However, this has not been studied extensively in vivo.
J Am Soc Echocardiogr
November 2004
Background: The development of therapeutic interventions to prevent progressive valve damage is more likely to limit the progression of structural damage to the aortic valve with normal function (aortic sclerosis [ASC]) than clinically apparent aortic stenosis. Currently, the ability to appreciate the progression of ASC is compromised by the subjective and qualitative evaluation of sclerosis severity.
Methods: We sought to reveal whether the intensity of ultrasonic backscatter could be used to quantify sclerosis severity in 26 patients with ASC and 23 healthy young adults.
Background: The coronary slow flow phenomenon (CSFP) is an angiographic finding characterized by Thrombolysis in Myocardial Infarction (TIMI)-2 flow in the absence of significant large vessel coronary disease. Although clinical and pathological features have been previously described, the underlying pathophysiology has not been fully elucidated. This study investigates the persistence of the phenomenon on serial angiographic studies, coronary hemodynamic findings at rest and during provocative stimuli, and biochemical evidence of inducible myocardial ischemia.
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