Potential role of coronary vasoconstriction in ischaemic heart disease: effect of exercise

Coronary vasomotion plays an important role in the regulation of coronary perfusion at rest and during exercise. Normal coronary arteries show coronary vasodilation of the proximal (+20%) and distal (+40%) vessel segments during supine bicycle exercise. However, patients with coronary artery disease show exercise-induced vasoconstriction of the stenotic vessel segments. The exact mechanism of exercise-induced stenosis narrowing is not clear but might be related to a passive collapse of the disease-free vessel wall (Venturi mechanism), elevated plasma levels of circulating catecholamines, an insufficient production of the endothelium-derived vesorelaxing factor or increased platelet aggregation due to turbulent blood flow with release of thromboxane A2 and serotonin. Various vasoactive drugs, such as nitroglycerin and calcium antagonists, prevent exercise-induced stenosis vasoconstriction. An additive effect on coronary vasodilation of the stenotic vessel segment was observed after combination of nitroglycerin with diltiazem. Thus, exercise-induced stenosis narrowing plays an important role in the pathophysiology of myocardial ischaemia during dynamic exercise. The antianginal effect of vasoactive substances can be explained—besides the effect on pre- and afterload—by a direct action on coronary stenosis vasomotio

Comparative validation of quantitative coronary angiography systems. Results and implications from a multicenter study using a standardized approach.

Background Computerized quantitative coronary angiography (QCA) has fundamentally altered our approach to the assessment of coronary interventional techniques and strategies aimed at the prevention of recurrence and progression of stenosis. It is essential, therefore, that the performance of QCA systems, upon which much of our scientific understanding has become integrally dependent, is evaluated in an objective and uniform manner. Methods and Results We validated 10 QCA systems at core laboratories in North America and Europe. Cine films were made of phantom stenoses of known diameter (0.5 to 1.9 mm)

Hämodynamik von Koronarstenosen

Under physiological conditions the resistance component of large epicardial coronary branches is very small in relation to total coronary resistance and can be neglected. The pressure losses across minor stenoses can be compensated by a decrease of resistance in the more peripheral coronary bed (autoregulation). This compensatory mechanism is limited to luminal obstructions less than 85%. Above this limit, when collateral vessels are not available, perfusion of the periphery becomes a function of the flow across the stenosis. As a consequence coronary reserve becomes abolished with an increasing obstruction. Coronary reserve describes an increase of coronary flow up to a factor of five, which, under normal conditions, is induced by dilation of resistors (arterioles) in the coronary bed. After exhaustion of coronary reserve the hemodynamic impact of a vascular narrowing can be expressed as the pressure loss across a coronary lesion (delta p). delta p is composed of viscous losses (AV) that are in linear relation to flow and inertial components that are related to the square of flow (B). Accordingly pressure loss across a stenosis can be expressed in a general form as delta p = AV X Q + B X Q2. In vitro data show that an approximation of delta p can be calculated on the basis of stenosis geometry including normal and minimal diameter, length, angle of entrance and exit, velocity of flow, viscosity and density of blood. Pressure losses across a stenosis can be divided in three components: the entrance, the narrow part, and the exit. Turbulence arises at the exit. This fact leads to a variable interaction of consecutive vascular lesions.(ABSTRACT TRUNCATED AT 250 WORDS

Potential role of coronary vasoconstriction in ischaemic heart disease: effect of exercise

Coronary vasomotion plays an important role in the regulation of coronary perfusion at rest and during exercise. Normal coronary arteries show coronary vasodilation of the proximal (+20%) and distal (+40%) vessel segments during supine bicycle exercise. However, patients with coronary artery disease show exercise-induced vasoconstriction of the stenotic vessel segments. The exact mechanism of exercise-induced stenosis narrowing is not clear but might be related to a passive collapse of the disease-free vessel wall (Venturi mechanism), elevated plasma levels of circulating catecholamines, an insufficient production of the endothelium-derived vesorelaxing factor or increased platelet aggregation due to turbulent blood flow with release of thromboxane A2 and serotonin. Various vasoactive drugs, such as nitroglycerin and calcium antagonists, prevent exercise-induced stenosis vasoconstriction. An additive effect on coronary vasodilation of the stenotic vessel segment was observed after combination of nitroglycerin with diltiazem. Thus, exercise-induced stenosis narrowing plays an important role in the pathophysiology of myocardial ischaemia during dynamic exercise. The antianginal effect of vasoactive substances can be explained—besides the effect on pre- and afterload—by a direct action on coronary stenosis vasomotio

Stress aortic valve index (SAVI) with dobutamine for low-gradient aortic stenosis: a pilot study

Background: Potentially some patients have symptoms that arise from their low-gradient aortic valve stenosis (AS). Comprehensive valve physiology with dobutamine stress remains incompletely characterized in this population. Methods: A cohort of 18 subjects with low-gradient AS underwent graded dobutamine infusion with invasive assessment using 0.014” pressure wires. A subset of 4 subjects received thermodilution cardiac output assessment at each stage. Results: Peak dobutamine hemodynamics could not be predicted from clinical or baseline parameters, reflecting statistically the physiologic heterogeneity of the measured pressure loss versus flow curves. While 0 subjects had a baseline aortic/left ventricular pressure ratio during ejection <0.71, 7 of 18 subjects (39%) achieved a ratio during peak dobutamine (the so-called stress aortic valve index, SAVI) below this threshold derived from a prior study of patients undergoing routine transcatheter aortic valve implantation (TAVI). Conclusion: For low-gradient AS, the hemodynamic changes from resting to peak dobutamine conditions cannot be predicted in advance due to pressure loss versus flow curve heterogeneity. A sizable minority of low-gradient AS reaches a severity during dobutamine stress equivalent to patients undergoing TAVI for established benefit. Whether this subset receives similar clinical advantage remains an unproven but natural hypothesis raised by our study