Harvey G. Kemp

The anginal syndrome associated with normal coronary arteriograms: Report of a six year experience

Abstract Although the occurrence of normal coronary arteriograms in patients with anginal pain is now recognized as a clinical entity, a large-scale study of such patients has not been reported. Accordingly, the historic aspects, laboratory findings and subsequent clinical course of 200 subjects (101 men and 99 women) with this syndrome were analyzed. Their average age was 47 years. No specific feature in the history could be discerned which separated these patients from those with angina due to coronary heart disease. The frequency of noncardiac sources of chest pain was similar in all patients. The electrocardiogram demonstrated abnormalities in the ST-T waves in slightly over 50 per cent of the patients, and the postexercise electrocardiogram was abnormal in another 20 per cent. Objective evidence for myocardial ischemia (myocardial lactate production) was three times more frequent in women than in men. The frequency of carbohydrate and/or lipid abnormalities was approximately half that in patients with coronary heart disease and did not correlate with the presence of myocardial ischemia. Long-term follow-up of these patients indicated that over half showed gradual improvement without specific therapy, whereas only 8 per cent had an increase in chest pain. Six patients died (four of unknown cause) in an average follow-up period of three years. Mortality, however, as determined by the life table method, was no greater than in a sex-age matched cohort derived from actuarial data. Although the etiology of this syndrome has not yet been demonstrated, its prognosis both in terms of persistence of pain and mortality appears to be benign.

Clinical studyThe anginal syndrome associated with normal coronary arteriograms: Report of a six year experience☆

Abstract Although the occurrence of normal coronary arteriograms in patients with anginal pain is now recognized as a clinical entity, a large-scale study of such patients has not been reported. Accordingly, the historic aspects, laboratory findings and subsequent clinical course of 200 subjects (101 men and 99 women) with this syndrome were analyzed. Their average age was 47 years. No specific feature in the history could be discerned which separated these patients from those with angina due to coronary heart disease. The frequency of noncardiac sources of chest pain was similar in all patients. The electrocardiogram demonstrated abnormalities in the ST-T waves in slightly over 50 per cent of the patients, and the postexercise electrocardiogram was abnormal in another 20 per cent. Objective evidence for myocardial ischemia (myocardial lactate production) was three times more frequent in women than in men. The frequency of carbohydrate and/or lipid abnormalities was approximately half that in patients with coronary heart disease and did not correlate with the presence of myocardial ischemia. Long-term follow-up of these patients indicated that over half showed gradual improvement without specific therapy, whereas only 8 per cent had an increase in chest pain. Six patients died (four of unknown cause) in an average follow-up period of three years. Mortality, however, as determined by the life table method, was no greater than in a sex-age matched cohort derived from actuarial data. Although the etiology of this syndrome has not yet been demonstrated, its prognosis both in terms of persistence of pain and mortality appears to be benign.

Progression of Coronary Artery Disease A Clinical Arteriographic Study

Significant progression of coronary artery disease was seen in 52% of subjects studied by selective cinearteriography at intervals between 2 and 75 months (average 23.8). Subsequent progression, although confined to proximal areas, was independent of overall severity of initial disease or previous disease at the site of progression and occurred frequently in previously normal vessels. Plasma lipid abnormalities and myocardial lactate production at the time of the initial study were significantly associated with subsequent arteriographic progression. Similarly abnormal glucose tolerance was seen more frequently in patients exhibiting progression than in those who did not. The progression occurring in patients with lipid abnormalities was more severe and more widespread than in other patients, and apparent interval reduction in lipid values did not influence the ultimate course of the atheromatous process. Myocardial infarction was almost invariably associated with progression. Collateral coronary circulation never increased or appeared unless accompanied by an increase in the extent of local coronary artery disease. The absence of progression was associated with a favorable prognosis. All other clinical, laboratory, and arteriographic parameters analyzed were not predictive of subsequent progression of the coronary obstructive lesion.

Propranolol and angina pectoris

Abstract Propranolol may offer an approach to the treatment of anginal pain which is refractory to conventional modes of therapy. Its efficacy may result from (1) lowering both left ventricular mechanical and metabolic requirements, (2) interference with sensory perception of anginal pain, or (3) blockade of adrenergic coronary vasoconstrictor activity which may precipitate angina in some subjects. Neither clinical nor resting physiologic data seem to be of value in predicting the response of a given patient to the drug.

Effects of Nitroglycerin on Regional Myocardial Blood Flow in Coronary Artery Disease

Regional myocardial blood flow before and after sublingual nitroglycerin was measured in 10 patients with coronary artery disease. During thoracotomy, (133)Xe was injected directly into the subepicardium in diseased regions of the anterior left ventricular wall, and washout rates were recorded with a scintillation counter. All disappearance curves were closely approximated by two exponential decays analyzed as two parallel flow systems by the compartmental method. The appearance of a double exponential decay pattern in diseased regions suggests that the slow phase was associated with collateral blood flow, although nonhomogeneous myocardium-to-blood partition coefficients for xenon cannot be excluded. Nitroglycerin increased the rapid phase flow in 9 of 10 patients and the slow flow in 7 of 10 patients. Average flow increased in 9 of the 10 patients (P < 0.01). Mean rapid phase flow in the control state was 110 ml/100 g per min and after nitroglycerin increased to 132 ml/100 g per min (P < 0.01); slow phase flow increased from 12 ml/100 g per min to 15 ml/100 g per min (P < 0.05). It is concluded that, under these conditions, nitroglycerin improves perfusion in regions of diseased myocardium in patients with coronary artery disease.

Coronary Atherosclerosis, Coronary Collaterals, and Their Relation to Cardiac Function

Abstract In subjects with coronary artery disease demonstrated by selective coronary arteriography there was a progressively higher prevalence of both ventriculographic abnormalities (asynergy) and...

Abnormalities of Ventricular Motion Induced by Atrial Pacing in Coronary Artery Disease

In order to study left ventricular performance and motion under ischemic stress, incremental atrial pacing was performed in 10 patients with angiographically proven coronary artery disease until angina pectoris or segmental S-T depression appeared. Single-plane left ventricular cineangiograms were obtained in both the resting and the transiently ischemic state induced by pacing.Abnormal motion appeared with pacing in two of three patients with normal contraction at rest; in one of them, gross dyskinesis of the cardiac apex was noted. Seven patients had abnormal contraction at rest; six showed an increase in either the severity or the topographic distribution of abnormality, while one showed no change.Left ventricular end-diastolic pressure and cardiac index were not altered significantly despite changes in the pattern of contraction. Left ventricular end-diastolic volume decreased irrespective of the development of asynergy, but ejection fraction decreased markedly in those patients in whom asynergy was induced de novo or increased.Thus left ventriculography during pacing-induced ischemia may reveal segmental or generalized abnormalities of contraction not necessarily reflected in the usual hemodynamic parameters of function. Moreover, asynergy induced by pacing is associated with a decreased ejection fraction.

Diagnostic Accuracy of Selective Coronary Cinearteriography

The premortem selective coronary cinearteriograms of 29 patients who subsequently died of their underlying disease have been compared to findings at postmortem examination. Only three errors of functional significance were found. Possible sources of these errors were analyzed. The most important single factor in determining the accuracy was the radiographic quality of the arteriogram. The data support the conclusion that selective coronary cinearteriography is a highly accurate means of evaluating the morphology of both normal and diseased coronary vessels, but high quality arteriograms and experienced interpreters are required.

Coronary Heart Disease Differential Hemodynamic, Metabolic, and Electrocardiographic Effects in Subjects With and Without Angina Pectoris During Atrial Pacing

Right atrial pacing was performed in 41 subjects with coronary heart disease. Twenty developed angina pectoris during pacing, while 21 did not. The extent of coronary artery disease, as judged by selective cinearteriography, was similar in the two groups. Both had significant increases in heart rate and pressure-time per minute, but there was no significant difference in either of these parameters between groups. Among the hemodynamic parameters measured, the only statistically significant change was in the cardiac index which fell slightly but significantly in the angina group.There were no differences in myocardial oxygen extraction either within each group or between groups. In the angina group, however, 14 of 20 subjects exhibited abnormal myocardial lactate metabolism during pacing. The mean change was highly significant (P < 0.01). In the nonangina group, eight of 21 subjects had abnormal lactate metabolism during pacing and the mean change was significant (P < 0.05). There was no correlation between abnormal lactate metabolism and electrocardiographic evidence of myocardial ischemia in either group. Sublingual nitroglycerin, given to five subjects with angina while pacing was continued, resulted in prompt relief of symptoms, but abnormal lactate metabolism and ST-segment depression were unaffected after 10 min. By contrast, when anginal symptoms were relieved in five subjects by cessation of pacing, symptomatic improvement was accompanied by marked improvement in lactate metabolism after 10 min. Although angina pectoris appears to be related statistically to subnormal left ventricular function and abnormal lactate metabolism, there is significant individual variation.

Atrial pacing in coronary heart disease. Effect on hemodynamics, metabolism and coronary circulation.

Abstract The effects of increased heart rate upon the physical and metabolic determinants of coronary blood flow in coronary heart disease provide a physiologic basis for the use of this investigative tool in cardiovascular studies. Heart rate increased by electrical pacing has minimal effects upon other hemodynamic indexes and arterial substrate concentrations, thus providing a considerable advantage over exercise and isoproterenol as a relatively uncomplicated myocardial stress. Atrial pacing represents a significant myocardial stress. Pressure-time per minute (PTM) increases with a nearly linear increase in myocardial oxygen consumption (MVO 2 ). This probably represents a balance between 2 unmeasured determinants of myocardial oxygen consumption, left ventricular size and contractility. If left ventricular failure supervenes, MVO 2 /PTM may rise rapidly. Although total coronary blood flow increases in a manner adequate to meet oxygen demand even in coronary heart disease, the presence of regional lactate production implies that this vasodilating capacity is exceeded in some areas or depths of the coronary vascular bed.