Myocardial ischemia induced by the cold pressor test in patients with exertion angina. Case contribution

The aim of the present study was to assess the incidence of myocardial ischemia during cold pressor test in patients with stable exertional angina pectoris. Thirty-seven patients with proven coronary artery disease were submitted to cold pressor and exercise stress testing; computer assisted electrocardiographic recordings were obtained throughout the examinations. Cold stimulation provoked electrocardiographic signs of subendocardial ischemia only in 3 patients. They had suffered of a previous myocardial infarction and showed low exercise tolerance and severe coronary lesions (one with triple vessel and 2 with left main disease). Interestingly, only one of these patients gave an history of angina during cold exposure. Thus these data indicate that chest pain and electrocardiographic signs of ischemia are an uncommon event during cold pressor stimulation which occurs more likely in patients with fairly severe coronary narrowings. More sensitive markers of ischemia and/or different modalities of cold application are required for studies concerning the relationship between cold exposure and angina pectoris.     

Cocaine-induced myocardial infarction in patients with normal coronary arteries

OBJECTIVE: To review the reported cases of myocardial infarction temporally related to recreational and topical anesthetic use of cocaine, with special regard for underlying etiologic factors in patients subsequently found to have normal coronary arteries. DATA SOURCES: Personal records of three cases and a comprehensive literature review using MEDLINE and supplemented by Index Medicus and the bibliographies of case reports. DATA SYNTHESIS: A total of 114 cases of cocaine-induced myocardial infarction were identified. The coronary anatomy was defined by angiography or autopsy in 92 patients, 38% of whom had normal coronary arteries. In these 35 patients (average age, 32; range, 21 to 60 years), myocardial infarction typically involved the anterior left ventricular wall (77%). Moderate cigarette smoking with one or fewer associated coronary risk factors was prevalent (68%). Focal coronary vasospasm was shown convincingly in only two cases. Intracoronary thrombus was initially found on 9 of 11 angiograms (82%) done within 12 hours of the myocardial infarction. Experimental evidence suggests that cocaine has direct and indirect sympathomimetic effects on vascular smooth muscle, attenuates endothelium vasodilator capacity, exerts a potent depressant effect on cardiac myocytes, and promotes atherogenesis. CONCLUSIONS: Cocaine-induced myocardial infarction in patients with normal coronary arteries probably involves adrenergically mediated increases in myocardial oxygen consumption, vasoconstriction of large epicardial arteries or small coronary resistance vessels, and coronary thrombosis. Accelerated atherosclerosis and impairment of endothelium vasodilator function may occur after chronic cocaine use.     

Importance of angina for development of collateral circulation

The extent of collateral circulation in 46 patients who had intracoronary thrombolysis within six hours of the onset of acute myocardial infarction was evaluated. Patients who had had a previous myocardial infarction (4 cases) or who had spontaneously recanalized infarct related coronary arteries (5 cases) were excluded from the analysis. Collateral development was graded during coronary cineangiography according to the extent of opacification of the collateral and epicardial arteries distal to the site of occlusion (collateral index 0 to 3). Angina was considered to be present before myocardial infarction if it had occurred more than one week before acute myocardial infarction. Collateral channels were visible in only two of 19 patients without angina before infarction and nine of the 18 patients with angina before infarction. The prevalence of angina and the collateral index were not significantly influenced by the extent of coronary vessel disease. It is concluded that myocardial ischaemia is important in promoting collateral development in man as well as in laboratory animals.     

Surgical versus non-surgical management of patients soon after acute myocardial infarction.

Of 510 patients admitted to hospital with acute myocardial infarction, 34 had coronary artery bypass grafting before discharge (6-43 days (median 20) after infarction). The patients who were given grafts generally had a smaller infarction with less functional impairment than the 476 patients who were not. The outcome of coronary artery bypass grafting was investigated in a retrospective matched pair study. Patients were matched on the basis of the presence of postinfarction angina, left ventricular ejection fraction, location of the infarction, peak creatine kinase activity, Killip clinical class, and severity of coronary disease with 34 patients who were given medical treatment only. At one year follow up fewer of the operated patients had symptoms than did the matched non-operated patients. Survival at one year in the operated and non-operated groups respectively was 94% vs 91%; angina within one year occurred in 3% vs 68%; congestive heart failure in 3% vs 6%; and 0% vs 32% were referred for later bypass grafting or coronary angioplasty. It is concluded that coronary artery bypass grafting can be performed safely soon after myocardial infarction provided that left ventricular function is not seriously compromised. Such treatment is more effective than medical treatment for relief of angina during the first year after infarction.     

Surgical versus non-surgical management of patients soon after acute myocardial infarction

Of 510 patients admitted to hospital with acute myocardial infarction, 34 had coronary artery bypass grafting before discharge (6-43 days (median 20) after infarction). The patients who were given grafts generally had a smaller infarction with less functional impairment than the 476 patients who were not. The outcome of coronary artery bypass grafting was investigated in a retrospective matched pair study. Patients were matched on the basis of the presence of postinfarction angina, left ventricular ejection fraction, location of the infarction, peak creatine kinase activity, Killip clinical class, and severity of coronary disease with 34 patients who were given medical treatment only. At one year follow up fewer of the operated patients had symptoms than did the matched non-operated patients. Survival at one year in the operated and non-operated groups respectively was 94% vs 91%; angina within one year occurred in 3% vs 68%; congestive heart failure in 3% vs 6%; and 0% vs 32% were referred for later bypass grafting or coronary angioplasty. It is concluded that coronary artery bypass grafting can be performed safely soon after myocardial infarction provided that left ventricular function is not seriously compromised. Such treatment is more effective than medical treatment for relief of angina during the first year after infarction.     

Importance of angina for development of collateral circulation.

The extent of collateral circulation in 46 patients who had intracoronary thrombolysis within six hours of the onset of acute myocardial infarction was evaluated. Patients who had had a previous myocardial infarction (4 cases) or who had spontaneously recanalized infarct related coronary arteries (5 cases) were excluded from the analysis. Collateral development was graded during coronary cineangiography according to the extent of opacification of the collateral and epicardial arteries distal to the site of occlusion (collateral index 0 to 3). Angina was considered to be present before myocardial infarction if it had occurred more than one week before acute myocardial infarction. Collateral channels were visible in only two of 19 patients without angina before infarction and nine of the 18 patients with angina before infarction. The prevalence of angina and the collateral index were not significantly influenced by the extent of coronary vessel disease. It is concluded that myocardial ischaemia is important in promoting collateral development in man as well as in laboratory animals.     

Cocaine-associated myocardial ischemia. Review of clinical and angiographic findings

The incidence of cocaine use is increasing in the United States among both adolescents and adults. Once thought to be a relatively safe street drug, cocaine has recently been implicated in 12 episodes of myocardial infarction. The case reports of these patients were retrospectively reviewed to determine the clinical and angiographic findings. All 12 patients exhibited electrocardiographic and angiographic evidence of myocardial infarction "shortly after" the use of cocaine by the nasal or intravenous routes. Most of the patients had fixed coronary artery disease. There appears to be increasing evidence of a temporal relationship between the use of cocaine and subsequent myocardial ischemic events in a subgroup of patients with or without fixed coronary artery stenosis. Physicians should inquire about cocaine use in patients with unexplained ischemic episodes since this may represent a potentially reversible factor in the later development of myocardial infarction.     

Coronary angioplasty for unstable angina: immediate and late results in 200 consecutive patients with identification of risk factors for unfavorable early and late outcome

Two hundred patients (mean age 56 years, range 36 to 74) with unstable angina (chest pain at rest, associated with ST-T changes) underwent coronary angioplasty. In 65 patients with multivessel disease, only the "culprit" lesion was dilated. The initial success rate was 89.5% (179 of 200 patients). At least one major procedure-related complication occurred in 21 patients (10.5%): (death in 1, myocardial infarction in 16 and urgent surgery in 18). All patients were followed up for 2 years. Five patients died late; 8 had a late nonfatal myocardial infarction and 52 had recurrence of angina pectoris. The restenosis rate was 32% (51 of 158) in the patients with initial successful angioplasty who had repeat angiography. At the 2 year follow-up, after attempted coronary angioplasty in all 200 patients, the total incidence rate of death was 3% (one procedure related; five late deaths), of nonfatal myocardial infarction 12% (16 procedure related and 8 late after angioplasty), and 13% (26 patients) were still symptomatic although they had improved in functional class. Multivariate analysis showed that variables indicating an increased risk 1) for major procedure-related complications were: ST segment elevation, persistent negative T wave and stenosis greater than or equal to 65% (odds ratio 3.7, 3.7 and 3.3, respectively); 2) for angiographic restenosis were: presence of collateral vessels, ST segment depression, multivessel disease, left anterior descending coronary artery stenosis and history of recent onset of symptoms (odds ratio: 2.2, 2.0, 1.9, 1.9 and 0.54, respectively); and 3) for late coronary events (recurrence of angina, late myocardial infarction or late death) were: multivessel disease, total occluded vessel and ST segment elevation (odds ratio 3.7, 2.8 and 0.44, respectively). Thus, coronary angioplasty for unstable angina can be performed with a high initial success rate, but at an increased risk of major complications. The prognosis is favorable after initial successful coronary angioplasty.     

Coronary angioplasty in unstable angina and stable angina: a comparison of success and complications

One hundred and five patients with unstable angina and 175 with chronic stable angina were treated by primary percutaneous transluminal coronary angioplasty. Patients with unstable angina had had symptoms for a shorter time and were more likely to have angiographically complex lesions and lesions less than 10 mm in length than patients with chronic stable angina. Other baseline variables were not significantly different in the two groups. The overall primary success rate was similar in both groups (87% v 86%). Nine of the 14 unsuccessful procedures in those with unstable angina and nine of the 24 unsuccessful procedures in those with stable angina were the result of acute occlusion. These results led to a 9% frequency of procedure related myocardial infarction in patients with unstable angina and a 5% rate in those with stable angina (NS). The procedure related infarct rate tended to be higher in patients with unstable angina who had coronary angioplasty soon after an episode of unstable angina (mean 10 days) than in those in whom it was delayed (mean 35 days) (12% v 3%) (NS). In patients with unstable angina who had had a previous myocardial infarction procedure related infarction was significantly more common (18%) than in patients with no previous myocardial infarction (3%). The difference between those with and without previous infarction was also significant in patients with stable angina (10% v 3%).     

ST-segment fluctuation during treadmill exercise in patients with angina pectoris

The level of the ST-segment fluctuates transiently during treadmill exercise in some patients with angina pectoris. In the present study, the incidence and clinical significance of ST-segment fluctuation were studied before and after propranolol in 52 patients with angina pectoris. A transient greater than 0.5-mm (0.05 mV) upward shift of the ST-segment during a graded treadmill test was considered a significant fluctuation in leads without signs of previous myocardial infarction. The fluctuation was observed in three of 30 patients with rest or rest and effort angina pectoris before propranolol and in 14 of them after propranolol, while only one of 22 patients with effort angina alone showed fluctuation after the drug. Coronary arteriography revealed that in 15 patients showing ST-segment fluctuation with propranolol, seven patients had no significant coronary stenosis, six had one-vessel disease and two had two-vessel disease. In 24 patients with documented coronary artery spasm, ST-segment fluctuation was induced in two (8%) before propranolol and in 13 (54%) after propranolol. Our results suggest that ST-segment fluctuation during graded treadmill exercise may be related to transient coronary vasospasms exacerbated by propranolol.     

Coronary angioplasty in unstable angina and stable angina: a comparison of success and complications.

One hundred and five patients with unstable angina and 175 with chronic stable angina were treated by primary percutaneous transluminal coronary angioplasty. Patients with unstable angina had had symptoms for a shorter time and were more likely to have angiographically complex lesions and lesions less than 10 mm in length than patients with chronic stable angina. Other baseline variables were not significantly different in the two groups. The overall primary success rate was similar in both groups (87% v 86%). Nine of the 14 unsuccessful procedures in those with unstable angina and nine of the 24 unsuccessful procedures in those with stable angina were the result of acute occlusion. These results led to a 9% frequency of procedure related myocardial infarction in patients with unstable angina and a 5% rate in those with stable angina (NS). The procedure related infarct rate tended to be higher in patients with unstable angina who had coronary angioplasty soon after an episode of unstable angina (mean 10 days) than in those in whom it was delayed (mean 35 days) (12% v 3%) (NS). In patients with unstable angina who had had a previous myocardial infarction procedure related infarction was significantly more common (18%) than in patients with no previous myocardial infarction (3%). The difference between those with and without previous infarction was also significant in patients with stable angina (10% v 3%).     

Coronary anatomy and arteriography in patients with unstable angina pectoris.

A prospective series of 188 patients with the syndrome of unstable angina pectoris undergoing coronary arteriography was reviewed to determine the spectrum of anatomic coronary artery disease, suitability for coronary revascularization and in-hospital morbidity and mortality. Thirty-two patients demonstrated normal to moderately diseased coronary arteries. None of these patients sustained myocardial infarction or died. Twenty patients (10.6 percent) had normal coronary arteriograms. Of the 156 patients having severe coronary artery disease (greater than 70 percent stenosis), 20 patients (13 percent) had left main coronary artery disease. One hundred forty-two patients (91 percent) were potential candidates for coronary surgery; 14 were not candidates because of distal vessel disease or poor left ventricular function. During cardiac angiography or in the subsequent hospital period 12 patients sustained a myocardial infarction and 7 of these died. Of these seven, six had left main coronary artery disease and one had three vessel disease. In three patients who died (1.9 percent of those with severe coronary artery disease) the death may have been related to cardiac catheterization because evidence of myocardial necrosis began within 24 hours of study. Thus, patients with the syndrome of unstable angina pectoris usually presented with severe coronary artery disease and were candidates for coronary revascularization. The anatomic severity of coronary artery disease appeared to be the most important factor contributing to myocardlal infarction or death after cardiac catheterization. Mortality after catheterization was primarily associated with left main coronary artery disease.     

Relationship of myocardial infarction to presence of angina pectoris in patients with coronary heart disease: Lack of abolition of angina by infarction

To evaluate the relationship between myocardial infarction and angina pectoris, history of symptomatic coronary heart disease was analyzed in 146 patients who had had documented myocardial infarction. There were 126 males and 70 females of mean age 55 years (range 32 to 70 years). Infarction had occurred 6 to 63 months prior to the study (mean: 30 months). Angina pectoris occurred at some time during the clinical course of 75 patients (51%), and 71 patients (49%) had not experienced angina. In the majority of the group with angina (n = 39; 52%) the symptom had not been present before infarction, appearing initially thereafter. Angina was present both before and after infarction in 31 patients (41%). In only 5 patients (7%) was precedent angina lost after infarction. Angina was, therefore, present in 70 of 146 patients (48%) after, compared to 36 patients (25%) before, infarction and in 86% (31/36) of patients with angina before infarction it persisted following the attack. Prior angina following myocardial infarction was not related to increased activity since in the majority of patients activity level was less after than before infarction. Post-infarction cardiac failure, which developed in 9 patients who had prior angina, was not associated with abolition of angina in any of this group. It is concluded that: 1. angina is frequent after myocardial infarction, 2. when present before infarction it usually persists thereafter, 3. angina commonly appears as a new symptom after infarction when not previously present and 4. disappearance of angina after infarction is distinctly uncommon.     

Clinical and angiographic assessment 6 months after double vessel percutaneous coronary angioplasty

Percutaneous transluminal coronary angioplasty is an accepted treatment for selected patients with single vessel disease but has not been rigorously evaluated in patients with double vessel disease. Among 769 patients undergoing transluminal coronary angioplasty between 1980 and 1984, 74 with double vessel stenosis of 50% or more underwent double vessel coronary angioplasty. Primary success was obtained for both lesions in 63 patients (85%), for one lesion in 11 patients (15%) and for 137 (93%) of 148 segments overall. Except for myocardial infarction in one patient, no serious complication occurred. Before coronary angioplasty, 15 patients had unstable angina, 14 had Canadian Cardiovascular Society class III and 32 class I to II effort angina and only 2 were asymptomatic. Six months after coronary angioplasty, 27 were asymptomatic, 27 had class I to II and 5 had class III effort angina and 2 had sustained an episode of unstable angina. During the follow-up study, two patients had an infarction and one had coronary artery bypass surgery. Coronary arteriography was performed at a mean of 5.5 +/- 2.1 months after coronary angioplasty in all but three patients. Restenosis was found in 30 (23%) of 132 segments with angiographic control. Restenosis was present in one vessel in 17 patients and in both vessels in 4; 40 patients (66%) had no restenosis. Of the 34 patients with definite or probable angina, 50% had restenosis and 19% of patients with restenosis were symptom free.(ABSTRACT TRUNCATED AT 250 WORDS)     

Arteriographic patterns early in the onset of the coronary syndromes.

Coronary arteriography in 300 patients within one year of onset of symptoms of coronary arterial disease revealed already severe anatomical coronary disease in three patient groups: those with angina pectoris alone (164 patients), with subendocardial myocardial infarction (63 patients), and with transmural myocardial infarction (73 patients). The number of vessels diseased (larger than or equal to 50% obstruction), distribution of obstruction, and degree of stenosis were similar in the three groups. However, total occlusion of at least one artery was much more common in transmural myocardial infarction and in subendocardial myocardial infarction with elevation of enzyme levels. We suggest that such occlusions occurred at the time of the infarction. Similarities in coronary anatomy between patient subgroups with angina (on exercise or at rest and nocturnal) indicate that factors other than coronary anatomy intervene in precipitating the different types of angina. Vessel disease was not related to smoking, hyperlipidaemia, or hypertension but coronary disease was manifest earlier in life in smokers or those with hyperlipidaemia.     

Arteriographic patterns early in the onset of the coronary syndromes.

Coronary arteriography in 300 patients within one year of onset of symptoms of coronary arterial disease revealed already severe anatomical coronary disease in three patient groups: those with angina pectoris alone (164 patients), with subendocardial myocardial infarction (63 patients), and with transmural myocardial infarction (73 patients). The number of vessels diseased (larger than or equal to 50% obstruction), distribution of obstruction, and degree of stenosis were similar in the three groups. However, total occlusion of at least one artery was much more common in transmural myocardial infarction and in subendocardial myocardial infarction with elevation of enzyme levels. We suggest that such occlusions occurred at the time of the infarction. Similarities in coronary anatomy between patient subgroups with angina (on exercise or at rest and nocturnal) indicate that factors other than coronary anatomy intervene in precipitating the different types of angina. Vessel disease was not related to smoking, hyperlipidaemia, or hypertension but coronary disease was manifest earlier in life in smokers or those with hyperlipidaemia.     

Mechanism of clinical onset and outcome of coronary disease before 40 years of age. 148 cases

This study reviewed the clinical histories of 148 coronary patients aged 34 +/- 5 years (20-40 years) documented in the same cardiology unit. Myocardial infarction was the presenting condition in 114 patients (77%): inaugural 65%, with prodrome 7%, asymptomatic 4%. The presentation was angina pectoris in 32 patients (22%): effort angina 15%, unstable angina 7%. Two patients had other symptoms (1%). The coronary lesions were significant (greater than 50%) in 112 patients (77%) which included 41% single vessel diseases and 36% multiple vessel diseases. The coronary lesions were insignificant in 10 patients (7%) and absent in 21 (15%) (33% under and 11% over 30 years of age). After an average follow-up of 48 months (range 1 to 10 years), 20 of the 32 patients presenting with angina developed myocardial infarction and 6 had episodes of unstable angina (65% in the first year following diagnosis). Six patients had no serious coronary events, but thereafter, 3 died. Fifteen patients (47%) are asymptomatic (including 8 after coronary bypass surgery). Ten patients are symptomatic. Of the 114 patients with inaugural myocardial infarction, 3 have died, 67 (58%) are symptomatic; the average number of risk factors per patient was related to age and to the degree of coronary artery disease. The left ventricular ejection fraction was significantly higher in asymptomatic patients than in those who had presented a coronary event after myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Rapid progression of coronary stenosis in patients with unstable angina pectoris selected for coronary angioplasty

We studied the course of coronary stenosis in the first 62 patients (45 men and 17 women) referred for coronary angioplasty in the interval between the diagnostic arteriogram and the preangioplasty coronary arteriogram. In 42 patients, the stenosis was in the left anterior descending artery, in 17 patients in the right coronary artery, in one patient in the left circumflex, and in two patients in the vein graft. Twenty-six patients had stable angina pectoris, 34 patients had unstable angina, and two patients had no angina. The coronary stenosis did not change significantly in any patient with stable angina. Conversely, the stenosis progressed in nine of the 34 patients with unstable angina (26.5%). In five of the nine patients with progression, total occlusion ensued. In four of the five patients total occlusion occurred within the 45-day interval between the diagnostic and the preangioplasty coronary arteriogram. New or increased preexisting collaterals to the occluded vessel developed in all five patients with total occlusion. None of these patients had clinical or electrocardiographic evidence of myocardial infarction or significant changes in ventricular function. Angiographic evidence of thrombi was seen in ten of 34 patients with unstable angina (29%). We concluded that coronary artery stenosis in patients with unstable angina pectoris is progressive in a significant number after a short time. The cause of progression of coronary stenosis in patients with unstable angina is unknown. Since in a significant number of patients with unstable angina coronary thrombus was suggested by angiography, coronary thrombosis superimposed on coronary atherosclerosis may play a significant role in this syndrome. Further prospective studies are needed, including repeat coronary arteriograms to evaluate the cause of unstable angina, define the role of coronary thrombosis, and evaluate the cause of unstable angina, define the role of coronary thrombosis, and evaluate the efficacy of more aggressive treatment adding the use of prolong heparin and antiplatelet agents prior to coronary angioplasty.     

Acute myocardial infarction temporally related to cocaine use. Clinical, angiographic, and pathophysiologic observations

Ischemic chest pain syndromes and myocardial infarction occurred within minutes to hours of cocaine use in nine persons ages 23 to 39 years. Five developed symptoms after taking cocaine intranasally; three, after intravenous use; and one, after smoking cocaine. Four were habitual users and five were recreational users; eight also smoked cigarettes heavily. Ischemic syndromes recurred in five who continued to use cocaine. Coronary arteriography showed an abnormal infarct-related vessel (more than 50% stenosis, total occlusion, or intraluminal thrombus) in seven patients. The noninfarct-related vessels were normal in eight patients. The left anterior descending coronary artery and the anteroapical left-ventricular wall were involved in all patients. After three patients had successful thrombolysis of the obstructed infarct-related vessel, angiography showed a normal underlying vessel.     

Early evolution of symptoms and long-term prognosis in variant angina: importance of the functional component of coronary arterial disease

PURPOSE: Most investigations describing the long-term outcome of large groups of patients with variant angina pectoris have focused on such endpoints as myocardial infarction, coronary artery surgery, and death, and have asked how the risk of these events is related to the severity of existing organic coronary disease. It is also possible to ask what is the relative importance of organic and functional components in causation of symptoms and outcomes, as was done in this study. PATIENTS AND METHODS: The early and long-term clinical course was observed in a group of 80 patients with variant angina and a low prevalence of severe organic coronary disease (diameter stenosis greater than 70 percent of one vessel in 28.3 percent, of two or more vessels in 2.7 percent). Patients were seen at the UCLA Medical Center between July 1963 and June 1985. RESULTS: The following observations were made: Compared with those experiencing a first episode of angina at rest, subjects whose first episode of vasospastic angina occurred during strenuous effort were more likely subsequently to have a positive exercise test result and a more stable but long-term anginal course. A good initial response to vasodilator therapy indicated a likelihood of being alive and symptom-free without an intervening myocardial infarction by five years after diagnosis, which was twice the rate as if initial response to such treatment was poor. The presence or absence of severe coronary artery obstruction as detected by angiography could not be predicted from the nature or severity of angina, the historical presence of effort angina, or the occurrence of a positive result on an exercise test. The existence of severe coronary stenosis in at least one vessel was not associated with an increased incidence of myocardial infarction, cardiac arrest, or death in the first nine years after diagnosis. CONCLUSION: These findings are consistent with the hypothesis that manifestations of ischemic heart disease in these patients were more directly caused by coronary vasospasm than by the degree of organic coronary obstruction seen by coronary arteriography. In addition, the presence of severe organic stenosis in one coronary artery did not appear to be associated with measurably increased adverse effects on clinical course or survival over the first nine years after diagnosis.