Haemodynamic and electrocardiographic accompaniments of resting postprandial angina.

Abstract

SUMMARY The early postprandial changes in 10 patients with angiographically proven coronary artery disease and history ofpostprandial angina were studied by the continuous recording on magnetic tape of the electrocardiogram and haemodynamic variables. The significant changes 20 minutes after a meal not followed by angina included increases in cardiac index and stroke index, with a decrease in systemic vascular resistance. When angina developed after a meal, there were significant increases in mean systemic arterial blood pressure, heart rate, pulmonary capillary wedge pressure, and systemic vascular resistance with decreases in stroke index at the onset of pain rather than at the onset of ischaemic electrocardiographic abnormalities. The first haemodynamic variable to change was pulmonary capillery wedge pressure which tended to increase coincident in time with the electrocardiographic abnormalities. In all cases, postprandial angina occurred within 25 minutes after a meal. In every instance, there was little or no change in the product of heart rate and systolic arterial blood pressure at the onset of the ischaemic electrocardiographic abnormalities at a time when the pulmonary capillary wedge pressure had begun to rise. Postprandial angina, like many cases of rest angina, may arise on the basis of a primary decrease in myocardial perfusion, the nature ofwhich is unclear but merits further investigation.

Regional Myocardial Blood Flow Redistribution as a Cause of Postprandial Angina Pectoris

“…An increase in cardiac work has also been suggested as a possible mechanism in postprandial angina. 2,5,6 In this study the standard liquid meal induced a significant increase in heart rate in postprandial angina patients 6,8 and in control subjects. 16,17 However, the magnitude of the rise in heart rate was not sufficient to produce a significant change in the rate-pressure product, a quantity known to increase linearly with myocardial oxygen consumption in normal subjects.…”

“…Others have suggested that an increase in cardiac work may have an important role in postprandial angina. 2,5,6 Indeed, the heart rate does increase after food both in normal subjects 7 and in patients with postprandial angina 6,8 ; however, the magnitude of this rise is not sufficient to cause a significant increase in myocardial oxygen consumption. 2,5,6 Evidence from previous studies suggests that stimuli increasing sympathetic nervous activity, such as increased heart rate, mental stress, and cold pressor, can reduce regional myocardial blood flow to below resting levels.…”

Gastrocardiac Afferent Convergence in Upper Thoracic Spinal Neurons: A Central Mechanism of Postprandial Angina Pectoris

“…These proposals include 1) a mechanical role on cardiac function 23 ; 2) postprandial redistribution of blood flow away from the coronary arteries and toward the gut (splanchnic vascular bed) or exercising muscles (in exertional postprandial angina) 4,6,25,48,50 ; 3) increased postprandial cardiac work and myocardial oxygen consumption after a meal 10,12,18 ; 4) a sympathetic reflex reduction in myocardial blood flow by coronary artery constriction and upregulation of the renin-angiotensin system secondary to postprandial gastric dilation or gastric receptor activation 4,15,32,46,47 ; 5) food ingestion-related release of gastrointestinal hormones into the circulation such as vasoactive intestinal peptides may modulate the cardiovascular responses to food intake 3,29,38 ; and 6) the influence of different dietary constituents that affect patients with angina. 3 All these proposals have weaknesses, as noted in the literature.…”

A Stress Repair Mechanism That Maintains Vertebrate Structure During Stress

“…Parasympathetic stimulation also releases insulin, which indirectly mobilizes nitric oxide in the capillaries of skeletal muscle and other peripheral tissues where parasympathetic innervation is absent [328,[336][337][338][339][340][341][342][343][344][345][346]. This explains why insulin prolongs bleeding time, reduces systemic vascular resistance, increases cardiac index, aggravates angina, and counteracts "vasopressor" (fibrinogenic) drugs; [307,310,311,329,341,[347][348][349][350] why allostatic load inhibits insulin effects; [351] and why diabetes and hypertension are closely-related [21, 202, 228, 229, 268-271, 273, 276-279, 311-313, 317-319, 346, 352-360].…”