Risk factors in the combination of myocardial infarction and carotid atheroma

This study compares two groups of patients: Group I with 44 patients who suffered recent acute myocardial infarction and Group II: 40 control subjects. In both groups, 2D Doppler echocardiography was performed to detect carotid atheroma, to determine the respective roles of vascular risk factors for two sites of atherosclerosis. Carotid atheroma affected 73 p. 100 of subjects in Group I and 22.5 p. 100 in Group II. Carotid stenosis of more than 40 p. 100 was found mainly in hypertensive patients who presented with acute myocardial infarction, and in patients with left ventricular hypertrophy. Smoking was more frequent in Group I than in Group II (p less than 0.001) irrespective of the frequency of carotid atheroma (p less than 0.05). Hypercholesterolaemia only favoured carotid atherosclerosis after acute myocardial infarction (p = 0.01). We did not find any difference in the incidence of diabetes mellitus in the two groups of patients. Age analysis indicated that carotid atheroma occurred earlier in Group I than in Group II. An association between a dominant risk factor for coronary disease (smoking or hypercholesterolemia) was found in 9 patients, all of whom had severe bipolar atherosclerosis with multivessel coronary lesions and carotid stenosis.     

The relationship between chest pain during thallium-201 scintigraphy with dipyridamole and myocardial ischemia

Dipyridamole thallium-201 scintigraphy (DP-Tl) and coronary angiography were studied on 74 patients with suspected coronary artery disease. We compared the clinical features, hemodynamic responses, angiographic results and scintigraphic findings of patients who had chest pain during DP-Tl testing ('chest pain' group) with those of patients who did not have chest pain ('no pain' group). Thirty eight (51%) of the 74 patients developed chest pain. Heart rate and rate pressure product during DP infusion of 'chest pain' group were greater than those of the 'no pain' group (p less than 0.05). Ischemic ST depression was more frequently observed among 'chest pain' patients (p less than 0.01). There were no differences in angiographic severity of coronary artery disease between 'chest pain' and 'no pain' group. Also, we could find no differences in extent and severity scores of perfusion defects and washout abnormalities between the two groups. However, when patients with myocardial infarction were excluded, the 'chest pain' group had significantly greater extent and severity scores of washout abnormalities than the 'no pain' group (extent score: 38 +/- 8 vs 18 +/- 5, p less than 0.05, severity score: 55 +/- 15 vs 18 +/- 7, p less than 0.01). Our study indicated that in patients without myocardial infarction, patients with 'chest pain' had more severe ischemia than 'no pain' patients. But in patients with myocardial infarction, myocardial ischemia not accompanied by chest pain might be as severe as that with chest pain. The presence or absence of myocardial infarction might have great influence on results regarding the relation of chest pain to myocardial ischemia.     

Stiffness of systemic arteries in patients with myocardial infarction. A noninvasive method to predict severity of coronary atherosclerosis

The static elastic properties of arterial tree (abdominal aorta and common carotid artery) were studied in 19 normal subjects and in 49 patients with myocardial infarction with an ultrasonic phase-locked echo-tracking system that allows continuous transcutaneous measurement of the arterial diameter. The stiffness index beta, which represented the mechanical properties in the arterial wall, was calculated from the relation between systemic blood pressure and the diameter of the artery. Patients with myocardial infarction underwent coronary angiography in their convalescent period to determine involved vessels. In 11 patients, coronary artery was patent; 15 patients had one-vessel disease, 12 had two-vessel disease, and the remaining 11 patients had three-vessel disease. In normal subjects, increasing age was associated with an increase in arterial stiffness. An average value of the stiffness index of the abdominal aorta was 8.58 +/- 3.02 (mean +/- SD) and that of common carotid artery was 9.17 +/- 2.22. In patients with three-vessel disease, these values were significantly higher (22.37 +/- 4.29 in abdominal aorta and 13.17 +/- 4.56 in common carotid artery) than those in normal subjects. Stiffness index of patients with two- or one-vessel disease was also increased but lower than those in patients with three-vessel disease (p less than 0.05). Forty-four of 49 patients with infarction had an arterial stiffness index of abdominal aorta higher than the 95% confidence limits of the normal data (p less than 0.05). Twenty-eight patients were outside the nomogram of common carotid artery (p less than 0.05). The mechanical properties of these elastic arteries provided sufficiently reliable information on changes caused by atherosclerosis.     

Right ventricular myocardial infarction in patients with chronic lung disease: possible role of right ventricular hypertrophy

To determine the relation between right ventricular hypertrophy and right ventricular myocardial infarction in patients with chronic lung disease, the records of 28 patients with chronic lung disease, inferior myocardial infarction and significant coronary artery disease (group I) and 20 patients with right ventricular hypertrophy, chronic lung disease without inferior myocardial infarction or significant coronary artery disease (group II) were reviewed. Chronic lung disease was diagnosed by clinical criteria, chest radiographs and pulmonary function tests. All patients had postmortem examinations. Patients in group I were classified into two subgroups: group Ia (without right ventricular hypertrophy) and group Ib (with right ventricular hypertrophy). Right ventricular wall thickness was 3.3 mm +/- 0.5 in group Ia, 6.0 mm +/- 1.1 in group Ib and 8.8 mm +/- 2.4 in group II (group Ia versus Ib, p less than 0.001; group Ia versus II, p less than 0.001; group Ib versus II, p less than 0.001). Eleven patients (78.6%) in group Ib (chronic lung disease with both right ventricular hypertrophy and inferior myocardial infarction) had right ventricular myocardial infarction compared with only 3 patients (21.9%) in group Ia (chronic lung disease without right ventricular hypertrophy and with inferior myocardial infarction) (p less than 0.008). Isolated right ventricular myocardial infarction occurred in four patients (20%) in group II (chronic lung disease with right ventricular hypertrophy, but without evidence of infarction of the left ventricle or significant coronary artery disease). There was no significant difference in the extent of anatomic coronary disease in groups Ia and Ib.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular mechanical efficiency in coronary artery disease

The effect of coronary artery disease and prior myocardial infarction on cardiac energetics was determined by measuring left ventricular myocardial blood flow, oxygen consumption (MVO2), efficiency and ejection phase indexes in 36 patients undergoing coronary arteriography. Eight control patients with normal coronary arteriograms and normal left ventricular function, 15 patients with coronary artery disease without prior myocardial infarction and 13 patients with coronary disease and prior myocardial infarction (greater than 6 months) were studied. Left ventricular efficiency was calculated from left ventricular work, myocardial blood flow (measured by clearance of intracoronary xenon-133), and aortic and coronary sinus oxygen content. Left ventricular volumes, mass and ejection phase indexes were measured by quantitative left ventriculography. Left ventricular myocardial blood flow per 100 g/min was reduced in patients with coronary artery disease (49.0 +/- 8; p less than 0.01) and in patients with myocardial infarction (51.6 +/- 10; p less than 0.05) compared with control subjects (62.4 +/- 16), but total left ventricular flow was not reduced because of increased left ventricular mass. As a result, MVO2 did not differ significantly for the three patient groups (control 13.3, coronary artery disease 14.0 and myocardial infarction 14.3 ml/min). In the patients with myocardial infarction, left ventricular work index was reduced (2.4 versus 4.0 kg X m/m2 per min in the control group; p less than 0.001), causing efficiency to be reduced (15.9 versus 28.8% in the control group; p less than 0.001). Decreased efficiency correlated with ejection fraction (r = 0.54), mean velocity of circumferential fiber shortening (MVcf) (r = 0.45) and mean percent chordal shortening (r = 0.43) (all p less than 0.01). These data indicate that in control patients with normal coronary arteriograms, left ventricular myocardial efficiency averages 29%; in patients with coronary disease without myocardial infarction, left ventricular MVO2 and efficiency are in the normal range; in patients with prior myocardial infarction, left ventricular efficiency is significantly reduced as a result of diminished left ventricular work and normal MVO2; and reduced efficiency after myocardial infarction correlates with reduced ejection phase indexes.     

Long-term prognosis after myocardial infarction in patients with previous coronary artery bypass surgery

A group of 205 patients hospitalized with myocardial infarction 2 to 162 months (mean 66) after bypass surgery and 205 control patients with myocardial infarction were compared and followed up for 34 +/- 25 months after hospital discharge. At baseline the postbypass group contained more men (p less than 0.03) and more patients with previous myocardial infarction (p less than 0.06), but the groups were otherwise comparable. Indexes of infarct size were lower in postbypass patients: sum of ST elevation, QRS score, peak serum creatine kinase (CK) (1,115 +/- 994 versus 1,780 +/- 1,647 IU/liter) and peak MB CK (all p less than or equal to 0.001). Postmyocardial infarction ejection fraction was 45 +/- 15% in the postbypass group and 43 +/- 15% in the control group (p = NS); in-hospital mortality rate was 4 and 5%, respectively (p = NS). When patent grafts were taken into account, the two groups were comparable in extent of coronary artery disease. At 5 years after discharge, cumulative mortality was similar in the postbypass and control groups (30 versus 25%, respectively, p = NS). However, postbypass patients had more reinfarctions (40 versus 23%, p = 0.007), more admissions for unstable angina (23 versus 18%, p = 0.04) and more revascularization procedures (34 versus 20%, p = 0.04) than did control patients. The total for these events at 5 years was 70% in the postbypass group and 49% in the control group (p = 0.001). Thus, although patients with previous bypass surgery who develop acute myocardial infarction have a smaller infarct, their subsequent survival is no better than that of other patients with acute myocardial infarction. They experience more reinfarctions and unstable angina. Previous bypass surgery is an important clinical marker for recurrent cardiac events after myocardial infarction.     

Comparison of risk factors in vasospastic angina without significant fixed coronary narrowing to significant fixed coronary narrowing and no vasospastic angina

To determine the importance of usual risk factors of coronary artery disease (CAD) in patients with coronary artery spasm, 40 patients with vasospastic angina (VA), normal or nearly normal coronary arteries and without previous myocardial infarction were compared with 2 control groups of 40 patients each, matched for age and sex: 1 group with CAD and 1 without heart disease. Ninety percent of patients with VA were cigarette smokers and 70% were heavy smokers (more than 20 cigarettes daily), compared with 53% and 33% in patients with CAD (p less than 0.001) and 30% and 15% in those without heart disease (p less than 0.001). Except for cigarette smoking, the risk factor profile of patients with VA appeared more like the profile of patients without heart disease than that of patients with CAD. The results suggest that cigarette smoking may play a role in CAD independent of atherosclerosis and possibly favoring coronary artery spasm.     

Clinical and angiographic features and prognostic significance of early postinfarction angina with and without electrocardiographic signs of transient ischemia

PURPOSE: The goal of the study was to characterize the clinical and angiographic characteristics and the prognostic significance of early postinfarction angina associated or unassociated with ST-T changes. PATIENTS AND METHODS: Four hundred forty-nine consecutive patients surviving an acute myocardial infarction and catheterized before hospital discharge were included. They were closely monitored in the coronary care unit and a 12-lead electrocardiogram (ECG) was promptly obtained before the administration of nitroglycerin whenever chest pain suggestive of ischemia occurred. Complete follow-up information was obtained for all patients a mean of 14 +/- 8 months after the qualifying infarction. RESULTS: Early postinfarction angina occurred in 164 patients. Transient ST-T changes were documented during pain in 79 patients and were absent in 85. Compared with patients without postinfarction angina, patients with angina without ST-T changes were older and had a more frequent past history of angina (42% versus 28%, p = 0.01). They also more often had a non-Q-wave myocardial infarction with lower peak creatine kinase blood level elevation. At angiography, patients with angina had more extensive coronary artery disease (1.9 +/- 0.8 diseased vessels per patient versus 1.6 +/- 0.8, p less than 0.05) and more left ventricular segments at jeopardy by a significant coronary artery stenosis (1.5 +/- 1.1 versus 1.2 +/- 1.1, p less than 0.05). The presence of ST-T changes during chest pain was associated with a further increase in the severity of coronary artery disease (2.1 +/- 0.8 diseased vessels per patient, p less than 0.05) and with a less well-developed collateral circulation (18% versus 34% of patients, p = 0.01) that was more often compromised by a coronary artery stenosis (22% versus 8% of patients, p = 0.008). In-hospital infarct extension occurred in 2% of patients without angina, 3.5% of patients with angina without ECG changes, and 28% of patients with angina and ST-T changes (p less than 0.01). The 2-year survival was similar in the first two groups (90% and 96%), and poorer (83%, p = 0.02) in patients with ST-T changes. Survival rates without myocardial infarction were respectively 80%, 78%, and 67% (p less than 0.004). CONCLUSION: A gradient in the severity of coronary artery disease and in the extent of myocardium at jeopardy exists from patients with no postinfarction angina to patients with angina and to patients with angina accompanied by ECG signs of ischemia. The presence of ST-T changes during pain indicates a much less favorable clinical outcome.     

C-reactive protein and the severity of atherosclerosis in myocardial infarction patients with stable angina pectoris.

BACKGROUND: Recent findings provide evidence for the importance of inflammatory processes in the pathogenesis of atherosclerosis. C-reactive protein was elevated in patients with peripheral artery disease, coronary heart disease and myocardial infarction compared to normal subjects. METHODS: In 1112 male and 299 female survivors of myocardial infarction (mean age +/- SD, men, 50.4 +/- 9.5, women, 56.1 +/- 9.3), we investigated whether plasma C-reactive protein concentration is associated with the severity of coronary heart disease and generalized pre-clinical or clinically manifest arteriopathy. The control group consisted of 326 male and 138 female individuals matched for age without clinical symptoms of coronary disease. The severity of arteriosclerotic changes was determined for the extra-cranial brain-supplying arteries, abdominal aorta, pelvis and leg arteries. In myocardial infarction patients coronary angiography was performed. Laboratory analyses included determination of C-reactive protein, fibrinogen, D-dimer, HDL-cholesterol, LDL-cholesterol and triglycerides. RESULTS: The following ranking of C-reactive protein concentrations was found: controls < or = patients after myocardial infarction without atherosclerosis < or = patients with myocardial infarction and pre-clinical atherosclerosis < or = patients with myocardial infarction and clinically manifest atherosclerosis. Additionally, our data showed a significant association between C-reactive protein concentrations and the angiographically detected degree of coronary heart disease. CONCLUSIONS: As C-reactive protein is a marker of inflammatory processes, our results in patients with clinically manifest and early pre-clinical atherosclerosis support the hypothesis that inflammatory processes in the vessel wall participate in atherogenesis. Moreover, they support the hypothesis of a causal relationship between an acute phase reaction and the pathogenesis of atherosclerosis in coronary arteries and other parts of the arterial vessel system.     

Transient left ventricular filling abnormalities (diastolic stunning) after acute myocardial infarction

A variety of experimental studies suggest that diastolic left ventricular (LV) function changes after acute myocardial infarction (AMI), but limited data exist on these changes in humans. To assess diastolic filling after AMI, 60 patients underwent Doppler echocardiographic examination within 24 hours of AMI. Of 54 patients who also underwent catheterization, 45 (83%) were successfully reperfused. A subgroup of 17 patients underwent a follow-up Doppler examination at 7 days after infarction, whereas 15 patients with stable exertional angina served as control subjects. There was no significant difference in age, gender, incidence of systemic hypertension or diabetes mellitus, heart rate, mean arterial pressure or severity of coronary artery disease between the infarct and control groups. The infarct group had a lower velocity time integral total (9.9 +/- 0.4 cm vs 12.0 +/- 0.9 cm, p less than 0.001), a lower velocity time integral E (5.8 +/- 0.3 cm vs 6.8 +/- 0.5 cm, p less than 0.01) and a lower velocity time integral 0.333 (3.5 +/- 0.4 cm vs 6.1 +/- 0.5 cm, p less than 0.01) than the control group. In addition, velocity time integral A/total was significantly greater in the infarction group (0.44 +/- 0.03 vs 0.35 +/- 0.04, p less than 0.01) compared to the control group. The follow-up subgroup showed an increase in velocity time integral total (p less than 0.01), velocity time integral E (p less than 0.05) and velocity time integral 0.333/total (p less than 0.05) over the first 7 days after infarction. The final recovery values at 7 days were not significantly different from those of the coronary artery disease group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ultrasonic correlates of common carotid atherosclerosis in patients with coronary artery disease

Increased intima-media thickness and plaque development in the extracranial carotid arteries reportedly correlate well with the prevalence of coronary artery diseases. The location of these atherosclerotic lesions in the carotid artery varies with age in patients with coronary artery atherosclerosis. Intima-media thickness, plaque, and calcification in the common carotid artery and bifurcation were assessed with high-resolution B-mode ultrasonography. Forty patients with severe atherosclerosis of the coronary artery and 56 healthy control subjects with no risk factors for coronary atherosclerosis were included in this study. The subjects were divided into a middle-age group (40-59 yr) and an old-age group (60-79 yr). In both groups, the intimamedia thickness in the patients was significantly higher than that in the controls. Intima-media thickness of at least 0.7 mm in the middle-age group and at least 1.0 mm in the old-age group was specific and positively predictive of coronary artery disease. Plaque (> 1.0 mm) and calcification were more significant in patients than in controls. In the middle-age group, intimamedia thickness in the common carotid artery was correlated with coronary atherosclerotic severity. Conversely, in the old-age group, the presence of plaque and calcification at the bifurcation was correlated with coronary atherosclerotic severity. The characteristic manifestation of the atherosclerotic lesion in the carotid artery varied with age in patients with coronary artery disease.     

Role of endothelial function and inflammation in patients with cardiovascular risk factors, with and without a history of myocardial infarction

BACKGROUND: Endothelial dysfunction and inflammation, in particular their lack of improvement after risk reduction, might better reflect advanced atherosclerosis than just the presence of risk factors. The aim of this study was to compare endothelial function and inflammatory parameters in high-risk patients who had no history of myocardial infarction and in patients in a stable phase after myocardial infarction. METHODS: We compared endothelial function of the brachial artery, measured using high-resolution ultrasound, in 45 patients with hyperlipidaemia (Group 1), and in 45 patients in a stable period after myocardial infarction (Group 2). Forty-five healthy individuals served as a control group (Group 3). RESULTS: Compared to patients with treated hyperlipidaemia, patients after myocardial infarction had lower values of total and LDL cholesterol (p = 0.015; 0.005) and homocysteine (p < 0.005), but marginally higher IL-6 levels (p = 0.1). Other measurements were comparable. However, flow-mediated dilation of the brachial artery was significantly diminished in patients after myocardial infarction (10.6 +/- 3.0; 5.9 +/- 4.0; 14.0 +/- 1.9% for Groups 1-3; ANOVA p = 0.0001; respectively). CONCLUSIONS: We found that patients with previous myocardial infarction have substantially lower endothelial function and increased some inflammatory parameters than patients with a similar level of atherosclerotic risk profile but without clinically evident coronary artery disease.     

Cardiac events after carotid endarterectomy: long-term results]

BACKGROUND: The aim of this study was to evaluate the incidence of late cardiac events in patients submitted to carotid endarterectomy (CEA), asymptomatic for coronary artery disease during the carotid surgical procedure. METHODS: During a period of 11 years, 162 patients (122 males, 40 females, mean age 68 +/- 12 years), asymptomatic for coronary artery disease and/or without sings of coronary artery disease at the cardiological screening, were submitted to CEA for symptomatic or severe (> or = 70%) carotid stenoses. Clinical follow-up was performed on 151 patients (93%), to identify the incidence of cardiac and neurological events and freedom from late death. The results of this group of patients (group A) were compared to those obtained during follow-up of 147 patients (133 males, 14 females, mean age 69 +/- 15 years) (group B) affected by coronary artery disease and submitted to combined CEA and coronary artery bypass grafting (CABG). RESULTS: During follow-up, in group A freedom from late death, cardiac death and adverse neurological events were 77 +/- 4.8, 86 +/- 4.4 and 87.3 +/- 4.5% at 9 years, respectively. Freedom from adverse neurological events in group A was similar to that registered in group B (86.4 +/- 5.6%, p = NS). The incidence of cumulative cardiac events and fatal cardiac events (myocardial infarction, sudden death, congestive heart failure) on the contrary, was higher in group A than in group B (13.2 vs 6.8%, p = 0.0424, and 7.9 vs 3.4%, p = 0.0446, respectively). CONCLUSIONS: In patients submitted to isolated CEA, although without symptoms or signs of coronary artery disease at the timing of the carotid procedure, the possibility of a severe coronary disease development during follow-up is not negligible: the incidence of late cardiac events may be higher than in patients with coronary artery disease corrected at the same time of the CEA procedure. These data suggest the opportunity of a systematic cardiological screening during follow-up in patients submitted to isolated CEA, although clinically asymptomatic for coronary artery disease at the timing of the vascular procedure, to improve the long-term survival.     

Angiographic findings after myocardial infarction in patients with previous bypass surgery: explanations for smaller infarcts in this group compared with control patients

The incidence of previous coronary artery bypass surgery (CABS) in patients with acute myocardial infarction admitted to our hospital has risen from 2.3% to 11.2% in 6 years. We compared infarct size and the angiographically determined cause of infarction in 52 control patients and in 52 consecutive patients with acute myocardial infarction at least 2 months after they had undergone CABS. Baseline characteristics were similar in both groups except for a higher incidence of preexisting Q waves in the post-CABS group (22 vs 10; p less than .05). Indexes of myocardial infarct size were smaller in the post-CABS group compared with those in control patients: peak creatine kinease (CK) level (IU/liter) 1113 +/- 1094 (mean +/- SD) vs 1824 +/- 1932 (p less than .01), peak CK-MB level (IU/liter) 173 +/- 230 vs 272 +/- 332 (p less than .02), peak summed ST segment elevation (mm) 3.5 +/- 4.8 vs 8.2 +/- 9.9 (p less than .005), and QRS score on days 7 to 10, 1.9 +/- 3.0 vs 4.3 +/- 3.4 (p less than .001). Postinfarction left ventricular ejection fraction was higher in the post-CABS group (53 +/- 13%) compared with that in control patients (47 +/- 12%; p less than .05). The incidence of total occlusion of the artery to the infarct zone was similar in the post-CABS and control patients (33 vs 27), as was the incidence of one-, two-, and three-vessel disease (artery plus graft). Collateral blood flow to the infarct zone was found in 27 post-CABS patients and in 23 control patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of propranolol, timolol and metoprolol on myocardial infarct size after experimental coronary artery occlusion

The effects of equiblocking doses of three beta-adrenergic blocking agents, propranolol, timolol and metoprolol, on myocardial infarct size were evaluated in 28 dogs after acute experimental coronary artery occlusion. Heart rate, arterial pressure and arterial free fatty acid concentration were measured in an attempt to evaluate their effects on the extent of myocardial injury. The zone at risk of infarction in each dog 1 minute after left anterior coronary artery occlusion was assessed by injecting highly radioactive albumin microspheres into the left atrium, and the hypoperfused zone was determined by autoradiography. After 15 minutes, the dogs were randomized into four groups: control dogs (n = 7), propranolol-treated dogs (1.2 mg/kg intravenously, n = 7), timolol-treated dogs (0.2 mg/kg intravenously, n = 7) and metoprolol-treated dogs (1.2 mg/kg intravenously, n = 7). After 6 hours, the dogs were killed. The left ventricle was sliced and stained with triphenyl-tetrazolium chloride for measurement on infarct size. The same slices were then autoradiographed for measurement of the hypoperfused zone. The percent of hypoperfused zone that evolved to infarction (the ratio of infarct size to hypoperfused zone) was 90.4 +/- 1.9% in the control group, 72.4 +/- 2.4% in the propranolol-treated dogs (p less than 0.05 versus control group); 57.9 +/- 4.4% in the timolol-treated dogs (p less than 0.01 versus control group; p less than 0.05 versus propranolol) and 54.4 +/- 3.7% in the metoprolol-treated dogs (p less than 0.01 versus control group; p less than 0.05 versus propranolol). Thus, propranolol, timolol and metoprolol reduced myocardial infarct size in dogs by 20, 36 and 40%, respectively, after experimental coronary artery occlusion. Metoprolol and timolol protected the ischemic myocardium more effectively than did propranolol.     

Changes in coronary angiography in young patients with myocardial infarction]

OBJECTIVE: To assess the coronariographic changes and left ventricular function of a group of young patients (pts) (less than 40 years) with myocardial infarction. DESIGN: Retrospective analysis on clinical data and cineangiography. SETTING: Patients studied in the Cardiology Department and Cardiothoracic Department of the Santa Marta Hospital in Lisbon. PATIENTS AND INTERVENTIONS: Sequential sample of 40 pts 39 male and one female submitted to coronariography after an acute myocardial infarction (mean age--34 +/- 3 years). MEASUREMENTS AND RESULTS: Twenty one pts had one vessel disease, 6 pts two vessel disease, 3 pts three vessel disease, 1 left main disease (2.5%) and 9 normal coronary arteries. More than a half (22) had a lesion on the left anterior descending artery (proximal in 12-30%), 13 a lesion on the right coronary artery (proximal in 3) and 8 on the circunflex coronary artery. There were 22 (55%) total occlusions (3 of the circunflex, 9 of the left anterior descending artery and 10 of the right coronary artery). Of these 8 were proximal. We divided the pts according to the regional contractility score in three groups. Most of them had a moderate decrease in contractility. Three pts had an apical aneurysm and 8 pts had apical discinesia. Three of these 11 pts had no significant coronary lesions, six had one vessel disease and 6 had a proximal lesion of the left anterior descending artery. The mean ejection was 53% and none was less than 30%. There was a statistical difference of score and ejection fraction between anterior and inferior myocardial infarctions (6.5 +/- 1.8 versus 7.8 +/- 1.6 e 48 +/- 11.6 versus 55.4 +/- 10.8), p less than 0.05 and between those with and without a proximal lesion of the anterior descending coronary artery (5.5 +/- 1.5 versus 7.9 +/- 1.5 and 41.4 +/- 7.9 versus 56.3 +/- 9.9), p less than 0.0005. Neverthless, when we tried to separate the pts with or without atherosclerotic lesions (6.9 +/- 1.7 versus 7.9 +/- 2.2 and 50.4 +/- 11 versus 54.8 +/- 14.3) or with and without multivessel disease (7.2 +/- 1.8 versus 6.7 +/- 1.9 and 52.9 +/- 12.2 versus 46.6 +/- 8.7), no statistical difference of score and ejection fraction was found. CONCLUSION: Young patients with myocardial infarction are predominantly males; - There is an important number of one vessel disease and in many patients no coronary significant lesions were found; - The functional changes depended more on the proximal location than on the number of diseased vessels.     

Are degenerative changes in the aortic valve an additional important marker of atherosclerosis?

BACKGROUND AND AIM: Degenerative changes of the mitral annulus are associated with atherosclerotic disease. It has recently been suggested that degenerative changes in the aortic valve may also be associated with atherosclerosis. The intima-media thickness of the carotid arteries has been used as one of the best and earliest markers of atherosclerosis. The aim of this study was to evaluate whether the additional presence of degenerative changes in the aortic valve in coronary patients with mitral annular degenerative disease reflects different degrees of intima-media thickness as assessed by carotid ultrasonography. METHODS: The study group included 55 patients admitted for myocardial infarction who presented with degenerative changes of the mitral annulus assessed by echocardiography. Exclusion criteria were moderate or severe valvular heart disease and chronic renal failure. All patients underwent echocardiography, cardiac Doppler and carotid ultrasonography. Based on the echocardiographic findings, two sub-groups were formed: 1--with degenerative changes of the aortic valve; and 2--without degenerative changes of the aortic valve. Carotid ultrasonography was performed with a 7.5-10 MHz linear transducer and the following parameters were evaluated: 1--bilateral measurement of intima-media thickness in the common carotid artery; 2-- incidence of atheromatous plaques in the carotid arteries, and 3--incidence of >50% lesion in the internal carotid arteries assessed by pulsed Doppler (Vmax >125 cm/s). RESULTS: Thirty-three patients (aged 71.6 +/- 7.1 years), 21 men and 12 women, did not present degenerative changes in the aortic valve. The other group consisted of 22 individuals (aged 72.9 +/- 6.8 years), 14 men and 8 women, who did have such changes. Differences in age and gender distribution between the two groups were not significant. Patients with degenerative aortic valve disease had greater intima-media thickness than the control group (1.6 +/- 0.3 mm versus 1.3 +/- 0.4 mm, p < 0.001). Fifteen (68%) patients with aortic degenerative disease had plaques in the carotid arteries compared to 11 (33%) patients in the control group (p < 0.05). No significant differences were found between the two groups regarding the incidence of >50% atherosclerotic lesion in the internal carotid artery (22% versus 12%; NS). CONCLUSIONS: Patients with degenerative changes in the aortic valve presented significantly greater intima-media thickness and a higher incidence of atherosclerotic plaques than the control group, suggesting that their presence may constitute an additional important marker of severity of atherosclerotic disease.     

Asymptomatic transient ST changes during ambulatory ECG monitoring in diabetic patients

The reported higher incidence of painless myocardial infarction in diabetic patients suggests that asymptomatic transient myocardial ischemia may also be frequent in diabetes. To explore this possibility 51 subjects with type II diabetes, aged 43 to 71 years (mean +/- SEM 56 +/- 8), 70 nondiabetic patients with coronary artery disease (mean age 55 +/- 5), and 40 nondiabetic patients without overt coronary disease (age 54 +/- 9) were studied. Thirty-eight of the 51 diabetic patients (74%) had evidence of associated coronary disease and 19 (37%) had evidence of previous myocardial infarction. All subjects underwent continuous 24-hour ambulatory ECG monitoring. In 18 of 51 diabetic patients 93 episodes (73% of the total number) of asymptomatic ST segment changes were recorded; the total number of symptomatic episodes was 36, and they were observed in seven patients (27%). Forty-eight (60%) asymptomatic and 32 symptomatic episodes of significant ST changes were found in nondiabetic patients with coronary artery disease. When patients with previous myocardial infarction were examined separately, asymptomatic episodes of significant ST changes were observed in 10 of 19 diabetic patients and in 5 of 25 nondiabetic patients with coronary artery disease (p less than 0.05). In an additional 28 diabetic patients who underwent exercise stress test, 15 exhibited an abnormal ECG response; however, only five of them (33%) were symptomatic. This study suggests that the incidence of transitory myocardial ischemia, as assessed by ambulatory ECG monitoring and exercise stress test, is higher in type II diabetic patients than in nondiabetic control subjects with coronary artery disease.     

Predictive value of aortic atherosclerosis detected by transoesophageal echocardiography for the presumption of coronary artery disease

The aim of this study was to determine the relationship between plaques of aortic atheroma detected by transoesophageal echocardiography and the condition of the coronary arteries at coronary angiography. Two hundred and seventeen consecutive patients were included for systematic transoesophageal echocardiography blinded to the results of coronary angiography. Significant coronary disease was defined as stenosis of at least 70% of the artery lumen. Aortic atherosclerosis was classified in four grades. The average age of the patients was 54.5 +/- 10.5 years. The sex ratio was 2.55 in favour of men. The average coronary score was 5 +/- 4.5 and the lesion index was 1.1 +/- 0.96. One hundred and fifty-nine patients had aortic atheroma, 73% of which (80 cases) were complex lesions. The descending aorta was the commonest site (91%) followed by the transverse (40% and ascending aorta (14%). When the ascending aorta was affected there was a very significant association with coronary artery disease (100% of cases). Sixty-one per cent of patients had lesions of one aortic segment, 28% had lesions of two aortic segments and in 10%, all three aortic segments were involved. The presence of aortic atheroma was correlated with coronary artery disease with a sensitivity and specificity of 86% and 76% respectively. The positive and negative predictive values were 81% and 31% respectively. Seventy-five per cent of patients with a coronary score of at least 7 had aortic atheroma with complex lesions in 47% of cases. The lesion index was significantly higher in this group when the coronary score was less than 7 (1.98 +/- 0.8 vs 0.65 +/- 0.7, p<0.00001). Patients with coronary artery disease have more complex lesions of the descending than of the ascending aorta (94 vs 25%). Significant coronary artery disease was correlated with the presence of aortic atheroma, especially of the ascending aorta. The specificity and positive predictive values were 100% but the negative predictive value was poor, irrespective of the aortic segment involved (32% for the ascending aorta, 36% for the transverse and 35% for the descending aorta). The authors conclude that transoesophageal echocardiography of the thoracic aorta is a good method of predicting severe coronary atherosclerotic disease.     

Brachial reactivity and extent of coronary artery disease in patients with first ST-elevation acute myocardial infarction

We examined peripheral endothelial function, as measured by brachial artery reactivity, in 49 stable patients with a first episode of acute ST-segment elevation myocardial infarction to examine the relation between extent of coronary disease and peripheral vascular reactivity. Brachial artery reactivity was assessed by ultrasound and flow-mediated dilation (FMD) was calculated as the change in brachial artery diameter after release of suprasystolic blood pressure cuff inflation. FMD was classified as abnormal in (< or =6%) 19 patients (group 1) and as normal in 30 patients (group 2). Average FMDs were 2 +/- 2% in group 1 and 11 +/- 4% in group 2. Patients in group 1 were older (62 +/- 5 vs 54 +/- 11 years, p = 0.02) and more often had a history of hypertension (n = 10, 52%, vs 6, 20%, p = 0.017). Patients with abnormal endothelial function (group 1) had a larger number of coronary obstructive (>or =50%) lesions (3.6 +/- 2.4 vs 2.0 +/- 1.7, p = 0.01) and more extensive coronary disease (1.9 +/- 0.8 vs 1.4 +/- 0.8 vessel disease, p = 0.05). In patients with 3-vessel disease, FMD was lower (4.0 +/- 1.8% vs 8.2 +/- 0.8%, p = 0.04) than in those with lesser coronary involvement. In conclusion, in patients with a first episode of ST-segment elevation myocardial infarction, there was a strong correlation between extent of coronary artery disease and brachial artery reactivity. Patients with localized coronary disease had relatively normal brachial reactivity, whereas those with diffuse coronary disease had more severe abnormal brachial artery reactivity.