Angiotensin-converting enzyme inhibitor therapy.
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Biomedical subjects
Publications and source records attributed to J Z Przybojewski.
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IgG and IgM anti-cardiolipin antibodies (ACA) were assayed by an ELISA technique in 86 patients with ischaemic heart disease (IHD) and compared to 124 healthy controls and to 62 patients with rheumatoid arthritis (RA) and 20 with tuberculosis (TB). IgG ACA levels in IHD, RA and TB were comparable and significantly higher than in controls (P less than 0.0001). IgM ACA was significantly higher in IHD and RA than controls (P less than 0.0001) but not TB (P = 0.045). The number of IHD patients with raised ACA (IgG and/or IgM) was significantly greater than in RA or TB. (chi 2 = 30.77, P less than 0.0001). ACA were raised in 80.2% IHD patients on one or more occasions during a 1-11 day (mean 4.7) hospital admission. There was no difference in either ACA levels or in the frequency of ACA elevation in patients with stable or unstable angina pectoris or myocardial infarction. We conclude that there is a strong association between IHD and ACA with potentially important therapeutic implications.
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A young woman with angiographically normal coronary arteries had asymptomatic iatrogenic catheter-induced dissection of her right coronary artery which was managed conservatively. Because of continuing chest pain despite therapy, over a year later she again underwent selective coronary arteriography; a Softip cardiovascular catheter (Angiomedics Inc., Minneapolis) was used without complication. This may be the first report of use of this catheter after previous iatrogenic coronary artery dissection caused by a more conventional type. It is also the first time that this catheter was employed in the RSA. The use of a Softip cardiovascular catheter may significantly reduce this complication of a common coronary angiography.
A 64-year-old white woman with moderately severe rheumatic mitral stenosis complicated by atrial fibrillation and recurrent systemic embolisation to the brain was found at operation to have a large 'free-floating' left atrial thrombus, as well as multiple left atrial appendage thrombi. These had not been detected by echocardiography. She also had significantly reduced left ventricular contractility on cine angiography, and right coronary artery atherosclerosis. She underwent successful mitral valve replacement and excision of the left atrial appendage.
A middle-aged urbanised black man with unstable angina pectoris showed unusual findings on serial resting ECGs recorded during episodes of chest pain, as well as during symptom-free intervals. The 'normal variant pattern', known to occur in blacks, was recorded in the absence of angina; in a white patient with chest pain it would have been considered as being due to a possible hyperacute myocardial infarction. During repeated episodes of severe angina, 'pseudonormalisation' of the 'normal variant pattern' was seen but the pointer to myocardial ischaemia was the simultaneous occurrence of ST-segment depression, Selective coronary arteriography delineated critical lesions in both the left anterior descending and dominant left circumflex coronary arteries. Coronary artery bypass surgery was successful. The importance of recognition of the 'normal variant pattern' in the black population in which the incidence of atherosclerotic coronary artery disease is rising, is emphasised.
A 65-year-old white man with severe symptomatic four-vessel atherosclerotic coronary artery disease underwent selective coronary arteriography. Two hours after this procedure he developed hypovolaemic shock secondary to the hyperosmolar contrast medium, as well as severe angina pectoris accompanied by myocardial ischaemia. This diagnosis was established with the aid of Swan-Ganz catheterisation and the patient was successfully managed with intravenous fluid replacement and emergency coronary artery bypass graft surgery. Pathophysiological aspects are discussed with comments on the possible prevention of such a potentially life-threatening complication of selective coronary angiography.
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Exercise-induced Q-waves were encountered in four Caucasian males presenting to the Cardiac Clinic, Tygerberg Hospital, with chest pain suggestive of angina pectoris. This phenomenon occurred in four out of a total of 1943 patients undergoing treadmill stress testing (Bruce Protocol) during a two-year period, giving an incidence of 0.21 percent of this ECG response. Two of the four patients (cases 1 and 2) were documented to have coronary atherosclerosis by selective coronary arteriography. One of these patients may well have been experiencing coronary vasospasm. One of the remaining two patients was a teenager whose exercise response was probably normal, whilst the last patient could have had ischemic heart disease (IHD). This most interesting and rare response to exercise (stress) testing is discussed, emphasis being placed on its incidence, mechanism and clinical significance in IHD and other conditions in clinical practice. Awareness of the occasional transient nature of "pathological" Q-waves, whether these occur at rest or during exercise, has an important bearing on such acute therapeutic interventions as intracoronary thrombolysis and percutaneous transluminal coronary angioplasty.
Death directly related to selective coronary arteriography in 5 patients with a history of unstable angina pectoris during the period 1975-1985 is reported. Four different cardiologists were involved. A feature common to all the cases was the presence of significant ostial stenosis of the left mainstem coronary artery (LMCA); 2 patients had haemodynamically important obstruction of a dominant right coronary artery (RCA) ostium, while 2 others had total occlusion in the proximal part of a dominant RCA. The RCA in the last case was angiographically normal and non-dominant. Collateral coronary blood flow was fairly sparse in most cases and in 4 left ventricular dysfunction of varying degree was present. All patients developed severe hypotension and electromechanical dissociation after arteriography while still in the cardiac catheterization laboratory. Resuscitation efforts were uniformly unsuccessful. Autopsy on 1 patient demonstrated extensive obstructive coronary atherosclerosis with a massive acute anterior myocardial infarction. Cardiac catheterization poses an extremely high risk for this subgroup of patients with LMCA disease, as does selective coronary arteriography. The possible role of catheter-provoked coronary vasospasm of the LMCA is suggested; a recently introduced soft-tipped cardiovascular catheter may be more appropriate in this setting.
An acute myocardial infarction in a young man when there was no fixed atherosclerotic lesion in the coronary arteries is reported. Soon after the myocardial infarction the patient was shown to have thrombosis in the anterior descending branch of the left coronary artery but this later disappeared. In view of recurrent angina pectoris, provocation tests were undertaken with ergometrine maleate, cold pressor and hyperventilation. Both the drug and the hyperventilation provoked coronary spasm accompanied by angina pectoris but no ECG evidence of ischaemia.
It is important to exclude coronary vasospasm, the mechanism responsible for so-called 'dynamic' coronary stenosis, when selecting of patients for percutaneous transluminal coronary angioplasty (PTCA). Although cine angiographic demonstration of this frequently fleeting entity can sometimes be difficult, a strong suspicion should be aroused by a carefully taken history. The danger of PTCA in these cases of Prinzmetal's variant angina, as well as the frustration often encountered in drug management, is high-lighted.
In a 51-year-old medical colleague with symptomatic atherosclerotic coronary artery disease, coronary arteriography delineated significant left mainstem, left anterior descending and left circumflex coronary artery lesions and cine angiography demonstrated normal left ventricular contractility. Aortocoronary saphenous vein bypass grafting was successful. The postoperative appearance of QS waves on the ECG suggested the possible complication of an acute transmural anteroseptal and anterolateral myocardial infarction (MI). However, this possibility was excluded by resting technetium-99m and thallium-201 scintiscans, as well as by a technetium-99m-gated blood pool scintiscan. The occurrence of acute pericarditis approximately 2 weeks after surgery made clinical evaluation more difficult. The ECG may represent a pseudo-MI pattern, the patient having suffered a post-pericardiotomy syndrome. The importance of excluding postoperative acute MI is stressed. The causes of the appearance of new Q waves after aortocoronary saphenous vein bypass graft surgery are briefly outlined.
A 60-year-old woman with mild hypertension and presumed ischaemic heart disease was followed up over a very long period on account of angina pectoris. Acute myocardial infarction (MI) was suspected on the basis of the history, ECG findings and serum enzyme values, but disproved by radioisotope investigation. Echocardiography demonstrated features of hypertrophic obstructive cardiomyopathy (HOCM), a diagnosis supported by cardiac catheterization and endomyocardial biopsy (EMB). Histological features of HOCM were absent from left ventricular EMB specimens despite a significant intraventricular gradient, but the right ventricular EMB demonstrated extensive changes of HOCM despite a small intraventricular gradient. Cardiac catheterization excluded previous MI and coronary artery disease. A further interesting feature was the development of congestive cardiac failure, which necessitated modification of her drug therapy).
A 32-year-old white woman presented with angina pectoris and an acute myocardial infarction (MI) complicated by congestive cardiac failure. Other symptoms and results of immunological investigation were highly suggestive of systemic lupus erythematosus (SLE). Thallium-201 scintigraphy confirmed an extensive MI, as initially suspected from an ECG. Cardiac catheterization delineated a poorly contracting left ventricle secondary to MI. Selective coronary angiography showed features suspicious of coronary arteritis involving the left anterior descending and left circumflex coronary arteries. Right ventricular endomyocardial biopsy failed to show any 'small-vessel disease', vasculitis or myocarditis. We suggest that the acute MI was caused by coronary arteritis due to SLE. Overview of the literature indicates that coronary arteritis is not as rare a complication of SLE as previously believed; however, acute MI is most unusual.
A 31-year-old doctor's wife suffered from severe unstable angina pectoris (AP) due to two large, heavily calcified masses involving the right coronary artery and the left anterior descending branch of the left coronary artery. The causes of the masses could not be determined with certainty, but in view of the history (which included the ingestion of large quantities of raw boerewors (traditional spiced sausage) and histopathological findings, we believe that they were coronary artery aneurysms which developed secondary to coronary arteritis many years previously. The possibility of echinococcal (hydatid) infection is also discussed. Cardiac surgery entailed total excision of both masses, together with sections of their accompanying coronary arteries which had become fibrotic as a result of the arteritis, and reestablishment of coronary blood flow by the insertion of two saphenous vein coronary artery bypass grafts. Her AP was dramatically relieved and she continues to be asymptomatic without taking anti-anginal drugs.
Three cases of arrhythmia-induced syncope in the elderly are reported. The patients all showed some features of the sick sinus syndrome and had aortic ejection murmurs. Ventricular tachycardia occurred in 2 patients. The importance of trying to record an arrhythmia during a syncopal attack is stressed, as are the adverse effects of many drugs commonly prescribed in this age group. The relationship between the arrhythmias found and their association with aortic stenosis are discussed.
A 43-year-old coloured man had no risk factors for atheromatous coronary artery disease but suffered two acute myocardial infarctions (MIs) in rapid succession. Serological reactions for previous syphilitic (luetic) infection were positive. Hypertrophic cardiomyopathy (HCM) without obstruction was verified, although right ventricular endomyocardial biopsy specimens did not demonstrate histological features of this disease. Extensive MI was verified on left ventricular cine angiography. Selective coronary arteriography showed that the coronary arterial tree was diffusely aneurysmal in the absence of any obstruction. We postulate that syphilitic coronary arteritis, in the absence of the more pathognomonic coronary ostial stenotic lesions, was present and may have predisposed to coronary thrombus formation and repeated acute MI. Recurrent coronary vasospasm, associated with the HCM, cannot be excluded with certainty.