Myocardial perfusion in silent myocardial ischemia: investigation by exercise stress myocardial tomography with thallium-201

To investigate myocardial perfusion in silent myocardial ischemia, we performed exercise stress myocardial tomography with thallium-201 (T1) in 85 patients with coronary artery disease (CAD). Exercise stress myocardial tomography was obtained both immediately after exercise and three hours later. Patients were classified into two groups according to the presence (Symptomatic Group, n = 36) or absence (Silent Group, n = 49) of chest pain during exercise stress. Clinical features (age, gender and history of myocardial infarction) and arteriographically determined severity of CAD were the same in both groups. The extent of myocardial ischemia (% Ischemia) estimated by exercise stress myocardial tomography was the same in each group (30 +/- 10% in Silent Group, 28 +/- 12% in Symptomatic Group, NS). The severity of exercise-induced myocardial ischemia was expressed as a minimal value of myocardial T1 washout rate (minimal WOR) of each patient. Although exercise heart rate was identical in both groups, minimal WOR in Silent Group was significantly higher than that of Symptomatic Group (4 +/- 10% vs -16 +/- 14%, p less than 0.001). The study in patients who exhibited both silent and symptomatic ischemia showed same results. These findings suggest that the severity of ischemia is a fundamental factor in determining the presence or absence of pain during exercise induced ischemia.     

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.     

Estimation of jeopardized left ventricular myocardium in symptomatic and silent ischemia as determined by iodine-123 phenylpentadecanoic acid rotational tomography

Whether patients with silent myocardial ischemia have a lesser mass of ischemic myocardium than patients with symptomatic ischemia is controversial. Forty-five patients with angiographic coronary artery disease (greater than or equal to 70% luminal diameter narrowing) were studied. All patients had ischemic patterns of myocardial uptake and clearance of the long-chain fatty acid perfusion/metabolic imaging agent iodine-123 phenylpentadecanoic acid after maximal exercise. Single-photon emission computed tomography was performed and 25 myocardial segments were analyzed using circumferential activity profile curves. The 21 patients with silent treadmill ischemia exercised longer than the 24 patients with painful treadmill ischemia (430 +/- 137 vs 337 +/- 96 seconds, p less than 0.01) and to a higher heart rate (138 +/- 21 vs 125 +/- 18 beats/min, p less than 0.05). Patients with treadmill silent ischemia had the same number of abnormally perfused myocardial segments as patients with painful treadmill ischemia (8.6 +/- 4.5 vs 6.5 +/- 4.1 segments, difference not significant) and the same number of reversibly ischemic myocardial segments (4.0 +/- 1.4 vs 4.2 +/- 3.0 segments, difference not significant). The angiographic severity and extent of coronary artery disease were similar in the 2 groups. Thus, in this selected group of patients, those with silent treadmill ischemia appear to have at least as great an extent of ischemic myocardium as patients with painful exertional ischemia.     

Altered myocardial perfusion in patients with angina pectoris or silent ischemia during exercise as assessed by quantitative thallium-201 single-photon emission computed tomography

The extent of abnormally perfused myocardium was compared in patients with and without chest pain during treadmill exercise from a large, relatively low-risk consecutive patient population (n = 356) referred for quantitative thallium-201 single-photon emission computed tomography (SPECT). All patients had concurrent coronary angiography. Patients were excluded if they had prior coronary angioplasty or bypass surgery. Tomographic images were assessed visually and from computer-generated polar maps. Chest pain during exercise was as frequent in patients with normal coronary arteries (12%) as in those with significant (greater than 50% stenosis) coronary artery disease (CAD) (14%). In the 219 patients with significant CAD, silent ischemia was fivefold more common than symptomatic ischemia (83% versus 17%, p = 0.0001). However, there were no differences in the extent, severity, or distribution of coronary stenoses in patients with silent or symptomatic ischemia. Our major observation was that the extent of quantified SPECT perfusion defects was nearly identical in patients with (20.9 +/- 15.9%) and without (20.5 +/- 15.6%) exertional chest pain. The sensitivity for detecting the presence of CAD was significantly improved with quantitative SPECT compared with stress electrocardiography (87% versus 65%, p = 0.0001). Although scintigraphic and electrocardiographic evidence of exercise-induced ischemia were comparable in patients with chest pain (67% versus 73%, respectively; p = NS), SPECT was superior to stress electrocardiography for detecting silent myocardial ischemia (52% versus 35%, respectively; p = 0.01). The majority of patients in this study with CAD who developed ischemia during exercise testing were asymptomatic, although they exhibited an angiographic profile and extent of abnormally perfused myocardium similar to those of patients with symptomatic ischemia. The prognostic significance of quantified perfusion defects detected by SPECT remains to be assessed.     

Midterm outcome of patients with asymptomatic restenosis after coronary balloon angioplasty.

Although many patients with restenosis after balloon coronary angioplasty have recurrence of angina, others remain asymptomatic. To assess the clinical implications of asymptomatic coronary restenosis, we analyzed clinical and angiographic characteristics of 277 consecutive patients with restenosis, 133 (48%) of whom were asymptomatic (group I) and 144 (52%) symptomatic (group II). Restenosis was documented 6 to 9 months after the index procedure, or earlier if angina recurred, and was defined as a greater than 50% lumen narrowing (visual estimation). Group I (asymptomatic group) included fewer female (9% vs. 18%, p less than 0.05) and hypertensive patients (38% vs. 56%, p less than 0.005) and more patients with a previous myocardial infarction (48% vs. 28%, p less than 0.05) and single-vessel disease (67% vs. 55%, p less than 0.05). Before angioplasty, symptoms had lasted for a shorter period (10 +/- 25 vs. 23 +/- 42 months, p less than 0.001), ischemia after a recent infarction was a more frequent indication (21% vs. 10%, p less than 0.05) and total revascularization more frequently obtained (74% vs. 63%, p less than 0.05) in group I than in group II patients. Only a normal blood pressure, previous myocardial infarction, single-vessel disease and a shorter duration of symptoms were independent correlates of asymptomatic restenosis. No differences were found in stenosis severity before angioplasty (90% in both groups) or after angioplasty (22% +/- 12% vs. 24% +/- 16%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of adenosine in pathogenesis of anginal pain

The intravenous infusion of adenosine provokes anginalike chest pain. To establish its origin, an intracoronary infusion of increasing adenosine concentrations was given in 22 patients with stable angina pectoris. During adenosine infusion, 20 patients had chest pain without electrocardiographic signs of ischemia. They all reported that the chest pain was similar to their usual anginal pain. In 10 of the 22 patients adenosine was also infused into the right atrium, but it never produced symptoms at the doses that had provoked chest pain during intracoronary infusion. In seven other patients, the intracoronary adenosine infusion was repeated after intravenous administration of aminophylline, an antagonist of adenosine P1-receptors. Aminophylline decreased the severity of adenosine-induced chest pain (assessed with a visual analog scale) from 42 +/- 22 to 23 +/- 17 mm (p less than 0.002). In the remaining five of the 22 patients, monitoring of blood oxygen saturation in the coronary sinus during intracoronary adenosine administration showed that maximum coronary vasodilation was achieved at doses lower than those responsible for chest pain. A single-blind, placebo-controlled, randomized trial of the effect of aminophylline on exercise-induced chest pain was also performed in 20 other patients with stable angina. Aminophylline, compared with placebo, decreased the severity of chest pain at peak exercise from 67 +/- 21 to 51 +/- 23 mm (p less than 0.02), despite the achievement of a similar degree of ST-segment depression. Finally, the effect of intravenous adenosine was compared in 10 patients with predominantly painful myocardial ischemia and in 10 patients with predominantly silent ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differences in coronary flow and myocardial metabolism at rest and during pacing between patients with obstructive and patients with nonobstructive hypertrophic cardiomyopathy

Fifty patients with hypertrophic cardiomyopathy underwent invasive study of coronary and myocardial hemodynamics in the basal state and during the stress of pacing. The 23 patients with basal obstruction (average left ventricular outflow gradient, 77 +/- 33 mm Hg; left ventricular systolic pressure, 196 +/- 33 mm Hg, mean +/- 1 SD) had significantly lower coronary resistance (0.85 +/- 0.18 versus 1.32 +/- 0.44 mm Hg X min/ml, p less than 0.001) and higher basal coronary flow (106 +/- 20 versus 80 +/- 25 ml/min, p less than 0.001) in the anterior left ventricle, associated with higher regional myocardial oxygen consumption (12.4 +/- 3.6 versus 8.9 +/- 3.3 ml oxygen/min, p less than 0.001) compared with the 27 patients without obstruction (mean left ventricular systolic pressure 134 +/- 18 mm Hg, p less than 0.001). Myocardial oxygen consumption and coronary blood flow were also significantly higher at paced heart rates of 100 and 130 beats/min (the anginal threshold for 41 of the 50 patients) in patients with obstruction compared with those without. In patients with obstruction, transmural coronary flow reserve was exhausted at a heart rate of 130 beats/min; higher heart rates resulted in more severe metabolic evidence of ischemia with all patients experiencing chest pain, associated with an actual increase in coronary resistance. Patients without obstruction also demonstrated evidence of ischemia at heart rates of 130 and 150 beats/min, with 25 of 27 patients experiencing chest pain. In this group, myocardial ischemia occurred at significantly lower coronary flow, higher coronary resistance and lower myocardial oxygen consumption, suggesting more severely impaired flow delivery in this group compared with those with obstruction. Abnormalities in myocardial oxygen extraction and marked elevation in filling pressures during stress were noted in both groups. Thus, obstruction to left ventricular outflow is associated with high left ventricular systolic pressure and oxygen consumption and therefore has important pathogenetic importance to the precipitation of ischemia in patients with hypertrophic cardiomyopathy. Patients without obstruction may have greater impairment in coronary flow delivery during stress.     

Functional significance of coronary collateral perfusion in preserving myocardial integrity

Coronary collateral perfusion to the completely obstructed coronary artery was evaluated by coronary cineangiography in 32 patients. In 13 patients, there was neither history of severe chest pain of longer than 30-min duration nor electrocardiographic evidence of a transmural myocardial infarction (Group I). Among patients undergoing intracoronary thrombolytic therapy for the completely occluded infarct-related coronary artery within 6 h after the onset of symptoms of the first acute myocardial infarction, 19 patients had a history of preinfarction angina (Group II). Collateral visualization (collateral index) was found to be significantly greater in Group I (2.5 +/- 0.5, SD) than in Group II (0.9 +/- 1.0) (p less than 0.01). Group I patients had a longer history of angina (25 +/- 25 months) than did Group II patients (17 +/- 18 months) (p = NS). These findings indicate that well-developed coronary collateral vessels preserve myocardial integrity upon acute coronary occlusion and that a long-standing angina indicative of myocardial ischemia may play an important role in developing collateral channels.     

Chest pain and "normal" coronary arteries--role of small coronary arteries

To study the mechanism of chest pain in patients with insignificant epicardial coronary artery disease, 50 patients underwent great cardiac vein (GCV) flow, oxygen content and lactate determinations at rest and during pacing, and left ventricular end-diastolic pressure (LVEDP) measurements at rest and after pacing. Twenty-four patients having typical chest discomfort during pacing demonstrated significantly lower increase in flow from baseline (36 +/- 18% versus 86 +/- 24%, p less than 0.001) and decrease in coronary resistance (-17 +/- 12% versus -43 +/- 7%, p less than 0.001) compared with 26 patients without pacing-induced chest pain, despite no significant difference in myocardial oxygen consumption (MVO2) between the 2 groups. Lactate consumption at a heart rate (HR) of 150 beats/min was significantly less (28.3 +/- 21.5 versus 51.3 +/- 35.8 mM X ml/min, p less than 0.001) and the increase in LVEDP from rest to after pacing was significantly greater (5 +/- 2 versus 1 +/- 2 mm Hg, p less than 0.001) in the chest pain group. After administration of ergonovine, 0.15 mg intravenously, to 46 of these patients, 31 had typical pain either at rest (1 patient) or during pacing. This group had significantly lower increase in flow (38 +/- 20% versus 107 +/- 38%, p less than 0.001), and decrease in coronary resistance (-16 +/- 12% versus -45 +/- 11%, p less than 0.001) compared with the 15 patients not having chest pain, despite no significant difference in MVO2 between the 2 groups. Patients with chest pain also had lower lactate consumption at a HR of 150 beats/min (39.2 +/- 23.6 versus 65.3 +/- 46.3 mM X ml/min, p less than 0.01), greater arterial-GCV oxygen difference (12.5 +/- 1.3 versus 11.6 +/- 1.0 ml O2/100 ml, p less than 0.05), and a more marked increase in LVEDP from rest to after pacing (11 +/- 3 versus 5 +/- 2 mm Hg, p less than 0.001). Quantitative coronary arteriography demonstrated no significant luminal narrowing of the epicardial coronary arteries in response to ergonovine. These data are consistent with the hypothesis that some patients with chest pain and angiographically normal epicardial coronary arteries have dynamic abnormalities of the small coronary arteries or coronary microcirculation that cause abnormal vasodilator reserve or vasoconstriction, resulting in myocardial ischemia and angina pectoris.     

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)     

Coronary angioplasty as primary therapy for acute myocardial infarction 6 to 48 hours after symptom onset: report of an initial experience

Recent randomized trials in acute myocardial infarction suggest that infarct size reduction need not be achieved for intravenous streptokinase to improve patient survival. If this is the case, attempts to achieve late revascularization may be justified. To assess the results of late primary coronary angioplasty performed in the setting of acute myocardial infarction, the clinical and angiographic data as well as hospital outcome of 139 consecutive patients treated with coronary angioplasty without prior thrombolytic therapy 6 to 48 h after the onset of chest pain (late group) were compared with those of 117 patients treated with primary angioplasty less than 6 h after the onset of chest pain (early group); time to angioplasty was assessed as a covariate of survival. In the 139 patients treated greater than or equal to 6 h after the onset of chest pain, the mean age (+/- SD) was 57 +/- 12 years and the median time to angioplasty was 15 h; 61% had multivessel disease, 14% were in cardiogenic shock and the mean left ventricular ejection fraction was 44 +/- 12%. Angioplasty was successful (final diameter stenosis less than 70% and Thrombolysis in Myocardial Infarction [TIMI] flow grade greater than or equal to 2) in 78% of patients. Successful angioplasty was associated with a 5.5% in-hospital mortality rate, whereas unsuccessful angioplasty was associated with a 43% hospital mortality rate (p less than 0.001). Multivariate testing in all patients identified four independent predictors of in-hospital death: cardiogenic shock (p less than 0.001), unsuccessful angioplasty (p = 0.001), ejection fraction less than or equal to 30% (p = 0.002) and patient age (p = 0.004).(ABSTRACT TRUNCATED AT 250 WORDS)     

ST monitoring for myocardial ischemia during and after coronary angioplasty

We performed 12-lead electrocardiographic monitoring in 97 patients during coronary angioplasty (PTCA) of a single vessel to correlate ischemic ST changes with clinical, angiographic and coronary hemodynamic variables and to determine the optimum lead or combination of leads for their detection. Ischemia (chest pain or ST change, group A) occurred in 79 patients (80%), but in only 15 of 23 patients (65%) with collaterals (p less than 0.05). Ischemia occurred more often in left anterior descending and left circumflex PTCA than right coronary PTCA, but pain was the only manifestation more often in left circumflex and right coronary PTCA. Ischemic ST change was silent in 16% and this proportion did not differ in clinical or angiographic groups except for diabetes with 3 of 5 (60%) having silent ischemia (p less than 0.05). Patients in group A (ischemia) compared to group B (no ischemia) had less severe lesions (85 +/- 9 vs 91 +/- 7%, p less than 0.01), higher transstenotic gradients (62 +/- 19 vs 53 +/- 9 mm Hg, p less than 0.05) and lower distal occluded pressures (24 +/- 11 vs 33 +/- 10 mm Hg, p less than 0.01), suggesting less collateral flow. Compared with a 12-lead electrocardiogram, the best single lead for detecting ST change during PTCA in each artery had a sensitivity of 80% and this increased to 93% using the best 2 leads. The best 3 leads (V3/III/V5 for left anterior descending and III/V2/V5 for right coronary and left circumflex) increased sensitivity to 100%.(ABSTRACT TRUNCATED AT 250 WORDS)     

Technetium-99m sestamibi tomography in patients with spontaneous chest pain: correlations with clinical, electrocardiographic and angiographic findings.

The sensitivity and specificity of technetium-99m hexakis-2-methoxy-2-isobutyl-isonitrile (sestamibi) single-photon emission computed tomographic (SPECT) imaging for the diagnosis of coronary artery disease were studied in 45 patients admitted to the hospital for clinical suspicion of unstable angina. Only patients without prior myocardial infarction were included and all patients had technetium-99m sestamibi injection and a 12-lead electrocardiogram (ECG) during and less than or equal to 4 h after an episode of chest pain. Coronary angiography performed in all patients during hospitalization showed significant coronary artery disease (greater than or equal to 50% luminal diameter reduction) in 26 of the 45 patients. The SPECT studies obtained after injection of technetium-99m sestamibi during an episode of spontaneous chest pain showed a sensitivity of 96% for the detection of coronary artery disease; the 12-lead ECG obtained at the time of the injection had a sensitivity of 35%. With the patient in the pain-free state, respective sensitivity values were 65% and 38%. Specificity for the radionuclide study was 79% during pain and 84% in the pain-free state; for the ECG, it was 74% both during and between episodes of pain. The site of the perfusion defect corresponded to the most severe coronary artery lesion in 88% of patients. The severity of the perfusion defect correlated with the extent of coronary artery disease: the defect score was 5.3 +/- 3.3 with one-vessel disease, 4.9 +/- 2.8 with two-vessel disease and 10.5 +/- 5.0 with three-vessel disease (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Role of perceptive threshold in myocardial infarction patients without previous angina

The purpose of this study is to clarify the mechanism of sudden onset myocardial infarction (MI) without previous angina and the relationship of MI without previous angina to the mechanism of onset of postinfarction asymptomatic myocardial ischemia. The mean initial time of ischemic pain in the upper arm under the tourniquet test was significantly prolonged in the MI patients without previous angina, compared with that for the MI patients with previous angina and normal control subjects, although there are some overlapping cases (74 +/- 37 sec versus 52 +/- 20 sec (p less than 0.01), and versus 56 +/- 15 sec (p less than 0.05), respectively). The tolerance time for ischemic pain also was similarly prolonged. There was no significant difference between the groups of MI patients (with and without previous angina) with respect to age, frequency of complications of diabetes mellitus, severity of coronary artery lesions or site of MI. The incidence of post-infarction myocardial ischemia was 50% for the previous angina group and 39.5% for the group without previous angina, but the frequency of asymptomatic ischemia was significantly higher in patients without previous angina, at 66.7%, than in those with previous angina, 32.3% (p less than 0.05). These results suggest that there is a close relationship between the mechanism of MI with sudden onset and that of asymptomatic myocardial ischemia during the pre- and post-infarction periods in patients with low sensitivity to pain.     

Exercise-induced ST segment elevation 2 weeks after uncomplicated myocardial infarction: contributing factors and prognostic significance

To define the prevalence and clinical significance of exercise-induced ST segment elevation during predischarge treadmill testing after uncomplicated acute myocardial infarction confirmed by serum MB creatine kinase (CK) activity, 241 consecutive patients were prospectively investigated with quantitative exercise thallium-201 scintigraphy, rest radionuclide ventriculography and coronary angiography at 10 +/- 3 days. All patients received customary care, and in none was thrombolytic therapy or emergency coronary angioplasty employed. Eighty-two patients (34%) had exercise-induced ST segment elevation of greater than or equal to 1 mm above rest baseline. These patients were similar to the 159 patients without this finding with respect to history of prior infarction, the Norris coronary prognostic index, exercise duration, metabolic equivalents (METs) achieved and peak heart rate-blood pressure product. The frequency of inducible myocardial ischemia and extent of angiographic coronary disease was also comparable in the two groups. Findings associated with larger infarct size and transmural extent of infarction were more common in patients with exercise-induced ST segment elevation than in those without, including higher peak CK values (1,235 +/- 1,037 versus 942 +/- 915 mumol/min per liter, p less than 0.026), lower left ventricular ejection fraction (43 +/- 12 versus 51 +/- 10%, p less than 0.001), a higher prevalence of pathologic Q waves in greater than or equal to 2 contiguous infarct-related leads (80 versus 55%, p less than 0.001), more persistent thallium-201 defects (2.2 +/- 1.1 versus 1.4 +/- 1.1, p less than 0.001), abnormally increased lung uptake of thallium (33 versus 18%, p less than 0.01) and a greater number of akinetic or dyskinetic segments (3.2 +/- 2.5 versus 1.4 +/- 1.9, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Usefulness of intravenous propranolol in predicting left anterior descending blood flow during anterior myocardial infarction

The effect of propranolol on precordial ST-segment elevation was studied in 24 patients with acute anterior myocardial infarction. The electrocardiographic response to the drug was correlated with the early angiographic appearance of the left anterior descending coronary artery (LAD). After a 30-minute observation period, intravenous propranolol (average dose 3.5 +/- 2.2 mg) was given a mean of 2.8 +/- 1.9 hours after the onset of persistent chest pain. Coronary angiography was performed 3.6 +/- 2.0 hours after the onset of symptoms. Patients were classified into 2 groups according to the angiographic findings. Group A consisted of 7 patients with a stenotic but patent LAD and 1 patient with excellent collateral blood flow to that area. Group B consisted of 16 patients with a completely occluded LAD and poor or absent collateral blood flow. Patients in group A showed a mean reduction in precordial ST-segment elevation of 77 +/- 18% and patients in group B showed a mean reduction of 13 +/- 14% (p less than 0.005). Left ventricular ejection fraction at discharge was 0.6 +/- 0.07 in group A and 0.37 +/- 0.08 in group B (p less than 0.001). Thus, the electrocardiographic response to intravenous propranolol given early in the course of acute anterior myocardial infarction predicts the presence of blood flow to the infarcting zone. The combination of residual blood flow and reduction of ST-segment elevation secondary to propranolol is associated with preservation of ventricular function.     

Effect of the collateral circulation on myocardial salvage in patients with acute myocardial infarction]

The effects of the extent of coronary collateral circulations, the duration of myocardial ischemia and recanalization of infarct-related vessels on left ventricular function were evaluated in 43 patients with acute anteroseptal myocardial infarction. All patients had complete occlusions of their proximal left anterior descending coronary arteries and were treated with intra-coronary thrombolytic therapy within 8 hours after the onset of their chest pain. The 43 patients were categorized in 4 groups based on the extent of their coronary collaterals in the early period of myocardial infarction and the results of thrombolysis. Group A consisted of 11 patients with well-developed collaterals who had successful thrombolysis. Group B was comprised of 14 patients with poorly developed or no collaterals, and successful thrombolysis. In group C, there were 9 patients with well-developed collaterals and unsuccessful thrombolysis. In group D, there were 9 patients who had poorly or not developed collaterals, and all had unsuccessful thrombolysis. Four weeks after the intervention, ejection fraction (EF) and regional wall motion (RWM) were calculated from the data of the left ventricular angiograms. There was no significant difference in patients' age, sex, nor in peak serum creatine kinase among the 4 groups or the duration of myocardial ischemia between groups A and B. Patients with successful thrombolysis (groups A and B) had significantly higher EF and preserved RWM of infarct areas compared to patients with unsuccessful thrombolysis (groups C and D, p less than 0.05). Thirteen patients with early reperfusion (within 4 hours after the onset of chest pain) had significantly higher EF and better RWM than did 12 patients with late reperfusion and 18 patients with unsuccessful thrombolysis (p less than 0.01). However, there was no significant correlation between the duration of myocardial ischemia and RWM of the infarct areas among 25 patients who had successful thrombolysis (r = -0.3, NS). Patients in group A had higher EF and better RWM of infarct areas than did patients in groups B, C and D (p less than 0.01). In addition, 3 patients with well-developed collaterals had good RWM despite late reperfusion which occurred more than 4 hours after the onset of symptoms. These results suggest that the extent of coronary collaterals during the early period of myocardial infarction and the time delay from the onset of symptoms to the initiation of thrombolytic therapy are important factors for the salvage of left ventricular function in patients with myocardial infarction.     

Dipyridamole-thallium 201 tomography following acute myocardial infarct: significance for stratifying cardiac risk factors

For the purpose of risk stratification 80 consecutive patients (mean age 58 +/- 7) with a chest pain syndrome after documented myocardial infarction underwent tomographic vasodilation-redistribution thallium-201 perfusion imaging, using 0.56 mg/kg intravenous dipyridamole. Tomograms were analyzed for size and location of reversible and fixed perfusion defects and correlated to angiographic characteristics, left ventricular ejection fraction and wall motion, collateral status, and 1-year prognosis as measured by cardiac events within 14 +/- 3 months. No serious side effects were noted with the diagnostic use of intravenous dipyridamole. According to the perfusion pattern three subgroups of post-infarction patients were identified: 1) by ischemia at a distance with redistribution in non-infarct related territories (n = 48), 2) by peri-infarctional ischemia with redistribution in the territory of the "infarct artery" (n = 9), and 3) by exclusively fixed defects without redistribution (n = 23). Ischemia at a distance was associated with a larger reversible defect than peri-infarctional ischemia (p less than 0.05) and the pattern without redistribution (p less than 0.005); the fixed defect size, however, was similar in all three subgroups. In addition, the severity of coronary artery disease (Gensini score and number of diseased vessels) and the degree of collateralization was higher in presence of a redistribution pattern (p less than 0.05), although no significant differences in global and regional function were noted as a function of thallium-201 redistribution.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular dysfunction in patients with angina pectoris, normal epicardial coronary arteries, and abnormal vasodilator reserve

Thirty-three patients with chest pain despite angiographically normal coronary arteries underwent both coronary flow studies during pacing and resting and exercise gated blood pool scintigraphy. During atrial pacing after administration of ergonovine, those patients developing their typical chest pain demonstrated significantly lower great cardiac vein flow (97 +/- 31 vs 150 +/- 33 ml/min, p less than .001), higher coronary resistance (1.27 +/- 0.43 vs 0.77 +/- 0.18 mm Hg/ml/min, p less than .005), and less lactate consumption (30.5 +/- 22.0 vs 69.7 +/- 41.1 mM . ml/min, p less than .005) and a higher left ventricular end-diastolic pressure after pacing (20 +/- 4 vs 12 +/- 1, p less than .001) compared with those without pain and in the absence of significant luminal narrowing of the epicardial coronary arteries. The 26 patients with abnormal vasodilator reserve demonstrated reduced left ventricular ejection fraction during exercise (58 +/- 8%) compared with the seven patients with appropriate vasodilator reserve (66 +/- 4%, p less than .05) and with a group of 52 control patients of similar age and sex distribution and free of known heart disease (66 +/- 10%, p less than .001). In addition, 12 of the 26 patients with abnormal vasodilator reserve demonstrated exercise-induced regional wall motion abnormalities. Many of these patients also manifested impaired left ventricular diastolic filling at rest compared with the control subjects (peak filling rate 2.6 +/- 0.7 vs 3.2 +/- 0.7 end-diastolic volume/sec, p less than .005). Thus, patients with chest pain resulting from abnormal vasodilator reserve demonstrate abnormalities of left ventricular systolic and diastolic function suggestive of myocardial ischemia.     

Effect of nitroglycerin on coronary collateral function during exercise evaluated by quantitative analysis of thallium-201 single photon emission computed tomography

A noninfarcted, entirely collateral-dependent myocardial region provides an opportunity to assess the effect of nitroglycerin on coronary collateral function during exercise. Stress thallium-201 computed tomography was performed in seven patients with effort angina and no history of myocardial infarction, both before and after nitroglycerin (0.3 mg). All patients had single-vessel disease with total or subtotal (99% with delay) occlusion of proximal left anterior descending coronary artery and well-developed collaterals. The pressure-rate product, mean blood pressure, and heart rate at peak exercise did not differ before and after nitroglycerin. The size of the perfusion defect and the severity of ischemia during exercise estimated by quantitative analysis of thallium-201 single photon emission computed tomography were significantly less after nitroglycerin administration (extent score: 23 +/- 17 vs 7 +/- 9, p less than 0.01; severity score: 20 +/- 22 vs 3 +/- 4, p less than 0.05). The pressure-rate products at peak exercise did not differ before and after nitroglycerin, which suggested that the reduction in perfusion defect size was unlikely to be the result of decreased myocardial oxygen consumption. These results suggest that nitroglycerin improved coronary collateral function during exercise and thus prevented exercise-induced myocardial ischemia.