Changes In Ventricular End-diastolic Pressure Research Articles

Increased intensity of contrast material immediately after late angioplasty of infarct-related coronary artery is associated with reduced ventricular volumes at six months

To assess the contribution of residual muscle perfusion in the infarcted territory to prevent ventricular remodeling, 24 patients with 1-vessel disease underwent coronary angiography and angioplasty of a critical left anterior descending coronary stenosis 18 ± 11 days after a first anterior myocardial infarction. The degree of stenosis was assessed using biplane quantitative angiography, whereas ventricular volumes, together with regional wall motion, were computed from single-plane ventriculography. Patients were reevaluated at 6 months after they had been subdivided according to the videointensity of the territory of the culprit vessel, as assessed from images obtained during main stem dye contrast injections before and immediately after angioplasty using a subtraction technique (group A, increased intensity [n = 15]; group B, no change [n = 9]), assuming that higher peak intensities reflect greater myocardial blood volume. There was a significant time · group interaction for ventricular volumes (diastolic, −13 ± 12% for group A vs +20 ± 24% for group B, p = 0.008; systolic, −15 ± 19% for group A vs +18 ± 36% for group B, p = 0.017), although no interaction was evident for the degree of resolution of coronary stenosis or the extent of recovery of regional dysfunction. The effects on volumes were paralleled by changes in ventricular end-diastolic pressure (−3 ± 7 mm Hg in group A vs +5 ± 6 mm Hg in group B, p = 0.006), although baseline clinical characteristics and medical regimen over the 6-month period were quite comparable between the 2 groups. In conclusion, despite late angioplasty of the culprit vessel, ventricular remodeling is prevented mainly when the procedure guarantees improved perfusion at the muscular level. The result is not necessarily mediated by recovery of regional systolic function.

Cardiac receptors: Normal and disturbed function

Widely distributed throughout the heart is a network of fibers connected to the medullary cardiovascular centers by nonmedullated vagal afferent fibers. When the traffic in these fibers is interrupted by vagal cooling, and the input from the arterial baroreceptors is prevented, the arterial blood pressure increases. Thus, these receptors act to inhibit tonically the vasomotor center. The receptors in the atria alter their rate of discharge with changes in atrial transmural pressure and contractility and are most active during end-inspiration and early expiration when the transmural pressure is maximal. The receptors in the ventricles respond to changes in ventricular end-diastolic pressure (preload), to the pressure generated during systole (afterload) and to changes in ventricular contractility. The cardiac mechanoreceptors have an equal or greater effect on the renal bed than the arterial mechanoreceptors and this effect is enhanced by hypercapnia. In animals, the cardiac mechanoreceptors have less control of the muscle vessels than the arterial mechanoreceptors, but the reverse is true in man. Both the cardiac and arterial mechanoreceptors can modulate the output of renin from the kidney, but the cardiac mechanoreceptors are more sensitive to small changes in blood volume. During coronary occlusion, in association with the bulging of the ischemic myocardium, the rate of discharge of these cardiac receptors is greatly increased.

Clinical observations on paired electrical stimulation of the heart: Effects on ventricular performance and heart rate

When the ventricle is electrically stimulated shortly after the termination of the refractory period, a propagated depolarization occurs which does not result in a clearly defined second ventricular contraction. A technic for repetitively delivering properly spaced paired electrical stimuli to the human heart is described, and the effects of paired electrical stimulation, or of coupled pacing, in ten patients are presented. By prolonging the period of time during which the ventricles were unresponsive to other stimuli, it was possible to reduce the heart rate. Slowing the heart rate was accomplished in two patients with rapid ventricular rates, associated in one with atrial fibrillation and in the other with atrial tachycardia. Paired electrical stimulation also augmented the contractile state of the myocardium. This augmentation was evidenced by increases in the rate of rise of intraventricular pressure, the mean systolic ejection rate and the rate of myocardial shortening, and is considered to be a form of sustained postextrasystolic potentiation. However, no consistent changes in ventricular end-diastolic pressure or cardiac output occurred. The potential clinical applications of this technic are discussed.

Hemodynamic determinants of the maximal rate of rise of left ventricular pressure.

The maximal rate of left ventricular pressure development (max. dp/dt) was measured in an areflexic preparation which permitted independent control of stroke volume, heart rate, and aortic pressure. Max. dp/dt increased as a result of elevating ventricular end-diastolic pressure. Elevating mean aortic pressure and increasing heart rate each resulted in a higher max. dp/dt without a change in ventricular end-diastolic pressure. Aortic diastolic pressure was shown to influence max. dp/dt in the absence of changes in ventricular end-diastolic pressure or contractility. Increasing contractility increased max. dp/dt while changing the manner of ventricular activation decreased max. dp/dt. These findings demonstrate that changes in max. dp/dt can and frequently do reflect changes in myocardial contractility. These data also indicate that max. dp/dt is a complex function, subject not only to extrinsically induced changes in contractility, but also to ventricular end-diastolic pressure, aortic diastolic pressure, the manner of ventricular activation, and intrinsic adjustments of contractility.