William A. Neill

Acute coronary insufficiency - coronary occlusion after intermittent ischemic attacks.

We used angiography in a prospective study of the coronary circulation in patients with acute coronary insufficiency. Reversible ST-T changes during the acute illness corresponded anatomically with severely narrowed coronary arteries (80 to 95 per cent stenosis). Angiograms repeated four months later showed new complete occlusions in nine of 30 severely stenotic arteries. Eight of the new occlusions occurred in severely narrowed arteries previously correlated with regional ST-T changes. Six patients had myocardial infarctions, five of which corresponded with the site of a new occlusion. These results provide indirect evidence that the acute coronary-insufficiency syndrome commonly represents intermittent transient coronary-artery occlusion and a threat of new permanent occlusion of the same artery. Myocardial infarction in these patients appeared to occur as a complication of the new occlusion.

Subendocardial ischemia provoked by tachycardia in conscious dogs with coronary stenosis

We investigated the effect that mild coronary stenosis exerts on the ability of the coronary circulation to compensate for the increased extravascular compression that occurs in the subendocardium during tachycardia. An electromagnetic flowmeter transducer and balloon cuff occluder were implanted on the left circumflex coronary artery in seven dogs, and experiments were performed 1 week later with the dogs under sedation but conscious. Stenosis of the left circumflex artery was produced by partial inflation of the cuff occluder. We determined coronary blood flow distribution by the radioactive microsphere technique, injection 200,000 15mu spheres into the left ventricular cavity during (1) a control period, (2) stenosis of the left circumflex artery and a normal heart rate, and (3) stenosis of the left circumflex artery and tachycardia. When the heart rate was normal, the degree of stenosis used caused no change in myocardial microsphere distribution but eliminated postocclusion reactive hyperemia. Thus, reserve coronary vasodilation compensated for the stenosis. With the degree of stenosis kept constant, an increase in heart rate to 196 beats/min caused a marked transmural shift in distribution of microspheres from subendocardium into subepicardium within the region of the left ventricle supplied by the left circumflex artery. There was no significant transmural shift in the region supplied by the uninvolved left anterior descending coronary artery. Myocardial lactate extraction decreased. These results suggest that when reserve coronary vasodilation has already been utilized to compensate for coronary stenosis, the increased extravascular coronary compression from tachycardia causes subendocardial ischemia and hypoxia.

Effect of Heart Rate on Coronary Blood Flow Distribution in Dogs

We investigated the hypothesis that tachycardia augments the time of systolic compression of coronary blood vessels and shifts coronary blood flow from the subendocardial (inner) to the subepicardial (outer) layer of the left ventricle. Coronary blood flow distribution was determined in tranquilized dogs by the radioactive microsphere technique, with injection of approximately 200,000 spheres, 15 , into the left ventricular chamber. During the control period (mean heart rate 73 beats/min), there were consistent differences in the sphere concentrations (blood flow) in different regions of the heart, and the inner layer of the left ventricle always received more spheres than its outer layer. The mean inner/outer sphere ratios were 1.26 for the free wall and 1.39 for the septal wall. Tachycardia (heart rates of 151 and 193 beats/min) induced by atrial pacing or administration of atropine increased total coronary blood flow but systematically altered its distribution: The increase in blood flow to the atria was much greater than that to the ventricles, and the inner/outer sphere ratio of the left ventricle decreased in proportion to the increase in heart rate. Although the redistribution of coronary blood flow was not accompanied by chemical signs of myocardial hypoxia in these normal dogs, we propose that the shift in blood flow away from the left ventricular inner layer is exaggerated in patients with coronary artery disease, resulting in subendocardial ischemia and hypoxia during tachycardia.

Myocardial Hypoxia as the Basis for Angina Pectoris in a Patient with Normal Coronary Arteriograms

Abstract Although coronary arteriograms of a 48-year-old woman with exertional chest pain typical of angina pectoris and an abnormal exercise electrocardiogram were normal, myocardial hypoxia and anaerobic metabolism were demonstrated during induced tachycardia and are proposed as the basis of the angina pectoris. A cause of impaired myocardial oxygen metabolism other than obstructive disease of visible coronary arteries is suggested.

Clinically suspect ischemic heart disease not corroborated by demonstrable coronary artery disease. Physiologic investigations and clinical course.

Abstract In 11 patients with angina pectoris and abnormal stress electrocardiograms, no narrowing or obstruction of coronary vessels was visible by selective cut film and coronary cinearteriography. One patient showed chemical evidence of myocardial hypoxia despite normal arteriograms. Similar evidence of impaired myocardial oxygen supply was absent in the remaining 10 patients. We found no abnormality in hemoglobin O 2 affinity which might jeopardize myocardial O 2 supply. The clinical course of these patients, including that during a 1 to 2 year followup period, has not been complicated by myocardial infarction or cardiac failure. In 5 symptoms have decreased.

Response of coronary circulation to cutaneous cold

Abstract The coronary and systemic hemodynamic responses to cutaneous cold stimulation were investigated in 25 patients. Nineteen had coronary heart disease and six had no evidence of coronary heart disease. Cutaneous cold increased systemic arterial and left ventricular end-diastolic blood pressures. Coronary blood flow increased in proportion to the increase in myocardial oxygen consumption, and there was no significant change in coronary blood arteriovenous oxygen difference. Cold provoked angina pectoris in five patients and chemical evidence of myocardial hypoxia in seven patients. We detected no difference in systemic or coronary circulatory responses in patients with a history of cold intolerance, and myocardial hypoxia appeared to be related to restricted coronary reserve rather than to a special effect of cold on myocardial metabolism or coronary vasomotion.

Effects of arterial hypoxemia and hyperoxia on oxygen availability for myocardial metabolism: Patients with and without coronary heart disease

Abstract Nineteen patients breathed different gas mixtures to induce arterial hypoxemia and hyperoxia. In 10 patients without heart disease, the level of coronary venous blood oxygen saturation fell during moderate arterial hypoxemia (O2 saturation 64 to 85 per cent) and rose during arterial blood hyperoxia. However, the coronary venous blood lactate/pyruvate concentration ratio ( L P v ) remained nearly constant, thereby providing evidence that the blood O2 changes did not reflect changes in O2 availability for myocardial metabolism. During severe arterial hypoxemia (O2 saturation 47 to 58 per cent), in 1 of 3 patients the myocardium produced lactate, which is a sign of supplementary anaerobic metabolism. In most of the 9 patients with coronary heart disease, the changes in coronary venous blood O2 saturation were similar to those in the control patients. However, exceptions occurred. In 3 patients with coronary heart disease, moderate arterial hypoxemia increased the L P v , thus suggesting myocardial hypoxia. In 2 of these, the myocardium produced lactate (anaerobic metabolism). L P v remained constant during hyperoxia; therefore, there is no evidence that the blood hyperoxia augmented myocardial O2 availability or relieved chronic myocardial hypoxia.

Changes in blood oxygen affinity and hemodynamics in anemic dogs

Abstract The effects of anemia on blood oxygen transport were studied using twelve adult male dogs (25–30 kg). Blood was sampled through indwelling catheters. Blood oxygen dissociation curves were constructed at 38 °C and corrected to pH 7.40. Measurements of cardiac output at rest and without anesthesia were made in eight of the dogs. Studies were conducted prior to anemia, during anemia and after recovery. The blood oxygen capacity was lowered from 16.9 ± 2.0 to 6.3 ± 2.3 vol % by bleeding and replacement of the removed plasma. The oxygen partial pressure required to saturate 50 % of the bloods hemoglobin (P 50 ) changed from a mean of 30.9 ± 0.9 mm Hg to a mean of 32.3 ± 1.4 mm Hg during anemia. The dogs were separated into two groups depending upon whether the blood P 50 increased. Six dogs (Group 1) increased their blood P 50 values more than one S.D. above their control values; the other six dogs (Group 2) had blood with average P 50 values during anemia within one S.D. of their mean values during the control period. The degree of anemia was the same in both groups; so was the increase (69%) in cardiac output during anemia. The P O 2 of mixed venous blood dropped during anemia from 41 to 32 mm Hg in Group 1 and from 46 to 27 mm Hg in Group 2. There was no significant difference in oxygen consumption between the control and the anemic studies in either group; the dogs which did not lower their blood oxygen affinities maintained the oxygen delivery to their tissues despite a lower mean capillary oxygen tension.

Corrected transposition of the great arteries masquerading as coronary artery disease.

Abstract A man with corrected transposition of the great arteries and associated “mitral” and aortic insufficiency survived for 50 years. The patient had angina pectoris and abnormal cardiac contour on chest roentgenogram, and for many years coronary artery disease with ventricular aneurysm was suspected. The correct diagnosis was made by cardiac catheterization and coronary arteriography.