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Previous studies have demonstrated a potential relationship between psychological stress and platelet activation, which may serve as a link between stress and myocardial infarction (MI). However, the possibility that personality traits associated with coronary heart disease may affect platelet activation has not been adequately investigated. The effect of a laboratory stressor (Type A Structured Interview (SI) and speech task) on platelet activation was assessed in 14 stable post-MI patients and 15 age-matched healthy men, using a standardized method of measuring plasma beta-thromboglobulin (BTG) levels. BTG levels were increased after the stressor (average change = 2.0 ng/ml, p = .005). Increases in BTG with stress were related to higher SI ratings of Potential for Hostility (r = .53, p = .004) and Type A behavior (r = .43, p = .02) but not to Cook-Medley-rated hostility scores. Increases in norepinephrine levels and in diastolic blood pressure were nonsignificantly related to increases in BTG levels (ps < .10), whereas increases in epinephrine levels were unrelated. Despite ceasing aspirin and other platelet inhibitors for 10 days before testing, individuals taking platelet inhibitors before the study had less change in BTG with stress (p = .05). However, after statistical adjustment for this factor, SI ratings of Potential for Hostility were still strongly related to increases in BTG with stress (adjusted r = .56, p = .002). Contrary to expectations, healthy men tended to have greater change in BTG with stress than post-MI patients (p = .06). These results indicate that acute stress increases BTG levels and that hostility is related to greater platelet reactivity, independent of any long term effects of platelet inhibition.

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The presence of significant coronary artery disease in individual vessels was assessed using thallium-201 single-photon emission computed tomography (SPECT) after intravenous dipyridamole. Coronary angiograms were analyzed using quantitative computer-assisted techniques in 81 men patients. Eleven men with a less than 3% probability of coronary artery disease were used as a control population. Three definitions of a hemodynamically significant coronary stenosis were studied independently: (1) a greater than 50% luminal diameter narrowing; (2) an absolute cross-sectional area less than or equal to 2.0 mm2; or (3) a greater than or equal to 70% cross-sectional area obstruction. Myocardial perfusion after dipyridamole was analyzed using the quantitative (polar map) method in 213 regions from the group with known coronary anatomy and using 33 regions from the group with a low likelihood of disease. Receiver operating characteristic curves were used to define the best cut-off point for the discrimination between normal and abnormal perfusion. When related to each of the three quantitative angiographic criteria, the optimum balance between sensitivity and specificity occurred at a defect size of greater than or equal to 8% for the left anterior descending artery, greater than or equal to 4% for the circumflex artery, and greater than 0% for the right coronary artery. Using a luminal diameter narrowing of greater than 50% to define the presence of significant coronary artery disease, these corresponded to respective sensitivities and specificities of 0.82 and 0.76 for the left anterior descending artery, 0.71 and 0.71 for the circumflex artery, and 0.76 and 0.82 for the right coronary artery. Thus analysis of receiver operator characteristic curves provides a means to define abnormalities for the SPECT polar map program after dipyridamole stress. Different definitions of coronary stenosis significance as determined by quantitative angiography did not substantially alter the results of the thallium imaging data and thus suggest that these definitions are functionally similar.

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The data reviewed above show that the ideal thrombolytic or thrombolytic plus anticoagulant regimen does not exist. Nor is it clear to me that one regimen is unequivocally better than another in regards to clinical outcome. Publication of the full results of the ISIS-3 study and completion of the TAPS study, the GUSTO study, the TIMI-4 study plus others only now in the planning phases, should help. This review will not stay current very long. These data do, however, give some guides to certain circumstances in which one regimen might be preferred over others. If economics is a compelling issue, as it may be in public hospitals on a fixed budget or in the developing world, streptokinase may be the best choice. For early application of thrombolytic therapy, such as at the site of infarct occurrence and in automotive and aerial ambulances, anistreplase may be preferred because of its ease of administration. Previous administration of streptokinase or anistreplase (within the period of 48 h to 6 months after prior use) militate against their use as does a recent streptococcal infection. Heightened concerns about bleeding risk, except intracranially, in the absence of absolute contraindication of fibrinolytic therapy, e.g. remote gastrointestinal hemorrhage or the expected imminent need for an invasive procedure, may lead to preference for alteplase over streptokinase or anistreplase. On the other hand, heightened concerns about intracranial hemorrhage may lead to preference for streptokinase over alteplase or anistreplase. Alteplase may be preferred over non-fibrin-selective agents in the treatment of patients when administration is begun more than three hours after the presumed onset of infarction. These considerations notwithstanding, it is crucial that debates over the best choice of a regimen must not be allowed to prolong the time before administration of an effective thrombolytic agent to a patient with evolving Q-wave infarction who is a good candidate for this therapy. This review may also become dated in the not-too-distant future because of expected further advances in thrombolytic regimen. Application of new antithrombotic regimens was noted above. Future thrombolytic and antithrombotic regimens may be "cocktails" of one or more thrombolytic agents plus more powerful antithrombotic and antiplatelet agents. New generations of thrombolytic agents may replace the current first and second generation agents now used. Combination thrombolytic and anti-fibrin antibody agents and mutant tissue-type plasminogen activators with lower affinity for plasminogen activator inhibitor and longer half-lives are being developed.(ABSTRACT TRUNCATED AT 400 WORDS)

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Vasoactive intestinal peptide (VIP) is a neurotransmitter that has been identified in epicardial coronary arteries. To evaluate the direct effect of VIP on coronary hemodynamics and blood flow, graded doses of VIP (0.01, 0.03, 0.10, and 0.30 micrograms/min) were infused into the left coronary artery of 7 patients at the time of diagnostic cardiac catheterization for chest pain syndromes. None of the patients had coronary stenoses greater than 50% during subsequent angiography. Coronary sinus VIP concentrations increased during each infusion (22 +/- 28 pg/ml at baseline to 109 +/- 22 pg/ml at 0.30 micrograms/min; p less than 0.05), but arterial VIP was elevated (39 +/- 29 pg/ml) only at the maximal dose of 0.30 micrograms/min. During all dosages of VIP, heart rate, right atrial and left ventricular end-diastolic pressure, and the heart rate x blood pressure product did not change. Moreover, neither mean aortic pressure nor left ventricular peak + dP/dt changed significantly at doses less than 0.30 micrograms/min; at 0.30 micrograms/min, mean aortic pressure decreased (97 +/- 15 to 90 +/- 15 mm Hg; p less than 0.05) and LV peak + dP/dt increased (1,621 +/- 230 to 1,801 +/- 226 mm Hg/s; p less than 0.05). Compared to baseline, the arterial-coronary sinus O2 content difference and myocardial O2 extraction diminished progressively at the 0.03, 0.10, and 0.30 micrograms/min doses of VIP (118 +/- 12 ml O2/L vs. 94 +/- 15, 70 +/- 9, and 61 +/- 26 ml O2/L, respectively, and 0.64 +/- 0.05 vs. 0.53 +/- 0.10, 0.38 +/- 0.06, and 0.34 +/- 0.15, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

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Reverse redistribution refers to a thallium-201 perfusion defect that develops or becomes more evident on delayed imaging compared with the initial image immediately after stress. To determine the diagnostic importance of reverse redistribution after intravenous dipyridamole, thallium-201 single photon emission computed tomography and quantitative coronary arteriography were performed in 90 men with angina pectoris. Of the 250 myocardial segments analyzed, reverse redistribution was present in 17 (7%). Minimal coronary cross-sectional area in proximal vessel segments was less than or equal to 2.0 mm2 more often in regions with transient perfusion abnormalities than in regions with reverse redistribution (66 vs 29%, p less than 0.05). Compared with regions exhibiting transient perfusion abnormalities, regions with reverse redistribution had larger proximal arterial diameters (1.9 +/- 1.1 vs 1.3 +/- 1.1 mm, p less than 0.001) and cross-sectional areas (3.9 +/- 3.1 vs 2.2 +/- 2.6 mm2, p less than 0.001). Coronary artery dimensions and relative stenosis severity did not differ between those regions with normal perfusion and those with reverse redistribution. Reverse redistribution detected by thallium-201 single photon emission computed tomographic imaging after dipyridamole is uncommon, appears to occur as frequently in normal subjects as in patients undergoing coronary arteriography and does not indicate the presence of severe coronary artery disease.

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Vasoactive intestinal polypeptide (VIP), a probable neurotransmitter, is present in the hearts of experimental animals and is a coronary vasodilator in dogs. We evaluated the coronary hemodynamic effects of intravenously infused VIP in 11 men at two rates that modestly raised circulating VIP concentrations. The decreases in coronary and systemic vascular resistances during the second infusion, 33 and 31%, respectively, were slightly but insignificantly greater than the 24% decrease in pulmonary vascular resistance. Coronary sinus levels of 6-keto-prostaglandin F1 alpha were not elevated during the infusions, and cyclooxygenase inhibition did not significantly blunt coronary vasodilation. However, myocardial oxygen uptake rose significantly during both infusions. To test for a direct coronary vasodilator effect, we infused VIP into the left coronary artery of four other men at four levels. The maximum decline in coronary vascular resistance was 46% and was not associated with an increase in myocardial oxygen uptake. We conclude that 1) intravenous administration of low to intermediate doses of VIP in humans is associated with substantial coronary vasodilation, 2) the coronary bed appears to be at least as responsive as other vascular beds, 3) the coronary vasodilation is due to both direct and indirect effects, and 4) the coronary vasodilation does not appear to be mediated by prostaglandins.

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This study was undertaken to determine whether Doppler measurements of systolic aortic and diastolic mitral blood flow velocities could reliably detect the presence of reversible myocardial perfusion defects during intravenous dipyridamole-thallium-201 imaging. In addition, the ability of dipyridamole-Doppler echocardiography to predict the presence of significant coronary artery disease (CAD) was evaluated. Baseline and post-dipyridamole Doppler studies were performed in 10 normal control subjects and 23 patients with CAD. Aortic peak velocity and acceleration increased from baseline to post-dipyridamole in normal subjects by 0.07 +/- 0.07 m/s (p = 0.016) and 2.1 +/- 2.0 m/s2 (p = 0.009), respectively. The ratio of early to late peak transmitral velocities decreased slightly in normal subjects, by 0.18 +/- 0.72 (difference not significant), whereas the ratio of early to late transmitral velocity-time integrals increased by 0.07 +/- 0.93 (difference not significant). The response of aortic velocity and acceleration to intravenous dipyridamole was not significantly different between normal subjects, patients without reversible thallium-201 perfusion defects and patients with reversible thallium-201 perfusion defects. Furthermore, only 3 of 14 subjects with reversible thallium-201 perfusion defects had abnormal (greater than 2 standard deviations from the mean) responses of aortic velocity or acceleration to intravenous dipyridamole. No patient had an abnormal response of the early to late mitral peak velocity ratio. In addition, the response of Doppler aortic and mitral indexes to intravenous dipyridamole was not able to identify the presence of significant CAD as assessed by quantitative coronary arteriography.(ABSTRACT TRUNCATED AT 250 WORDS)

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A phantom was devised to validate scintigraphically determined left ventricular ejection fractions (LVEFs) and cardiac chamber volumes in the following simulated cardiac situations: normal contraction, moderately impaired left ventricular contraction, severely impaired left ventricular contraction, mitral regurgitation, and cardiomyopathy. The phantom, assembled from anatomically realistic cardiac chambers, simulated contraction and expansion using individual chamber pumps coordinated by a microcomputer. Scintigraphic studies were performed by sequential imaging of [99mTc]pertechnetate introduced into each chamber. The images were analyzed like conventional clinical studies, using both automatic and manual techniques. Scintigraphic techniques correlated with chamber volumes that were determined by weight to yield the following regression formulae: LVEF (by automatic method 1) = 1.08 x LVEF (by weight) -5.11; LVEF (by automatic method 2) = 1.00 x LVEF (by weight) -3.15; and LVEF (by manual method) = 1.04 x LVEF (by weight) -5.08 ml (Correlation coefficients greater than 0.98). The absolute left ventricular volumes (LVVs), determined by scintigraphy, correlated well with LVVs determined by weight. These correlations were performed with separations between the center of the left ventricle and the collimator varying from 5 cm to 9 cm. The regression formulae for 5, 7, and 9 cm distances were: LVV (by counts) = 0.99 x LVV (by weight) + 0.13, LVV (by counts) = 1.04 x LVV (by weight) + 9.08, LVV (by counts) = 0.88 x LVV (by weight) + 15.25, respectively. At 9 cm, slight volumetric underestimation occurred, as predicted from the work of Fearnow et al., possibly because of oversubtraction of background. Thus, this phantom provides a useful tool for validating scintigraphic cardiac blood-pool studies simulating a wide range of clinically relevant situations.

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Correcting for the attenuation of photons between the cardiac chambers and chest surface is crucial for accurate nongeometric ventricular volume determinations from equilibrium radionuclide angiograms. Previous techniques have assumed that the attenuation coefficient of water for 99mTc (0.15/cm) should be used for this correction. In this study, this assumption was tested directly by measuring attenuation of the activity of a radioactive source within the right and left cardiac chambers. The balloon of a flow-directed catheter, filled with 99mTc, was used as a source and its depth within the body was measured with biplane fluoroscopy. In ten patients, a total of 36 measurements of attenuation were made. With linear regression analysis, the overall calculated attenuation coefficient, mu, was 0.12/cm (standard error of slope = 0.01, R = 0.93). Although the mean value of mu varied from 0.08 to 0.13 for four different intracardiac locations these differences were not significant. These direct measurements indicate that the attenuation of photons in the heart is not equivalent to that of water and suggest that an attenuation coefficient of 0.12/cm should be used in analyzing ventricular activity.

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Unstable angina pectoris as a distinct syndrome intermediate between chronic stable angina and acute myocardial infarction was first described about a half century ago. The incidence of death or myocardial infarction rises in the first few months after destabilization of angina. Hemodynamic, scintigraphic, and arteriographic studies in the last 15 years have shown that unstable angina is chiefly due to "dynamic" coronary stenoses, transient reversible limitations in coronary blood flow caused by a complex interaction between coronary vasoconstriction, transient platelet plugging, and transient thrombosis. The trigger for the onset of dynamic coronary stenoses is probably acute changes in coronary arterial morphology in or near atherosclerotic plaques making those areas more thrombogenic. A large fraction of patients with unstable angina restabilize initially with medical management. The role of beta blockers is unclear, but they may protect against development of coronary events for patients with unstable angina similar to that reported for patients with myocardial infarction. Nitrates and calcium blockers are probably superior to beta blockers in restabilization of angina, but protection against coronary events has not yet been demonstrated clearly. Further investigation is needed to distinguish the relative benefits of a two-drug (heart rate-limiting calcium blocker plus nitrates) regimen vs. a three-drug regimen including beta blocker. There is no basis for emergency coronary bypass surgery to prevent myocardial infarction or death. Urgent surgery should be limited to patients who do not stabilize readily with medical therapy. One third or more of the patients who initially restabilize with medical therapy will require coronary revascularization in the year after unstable angina because of severe angina. An antithrombotic regimen of aspirin (or possibly heparin) reduces the incidence of progression to death or myocardial infarction. Two important future directions for research should be promising: development of better antithrombotic regimens other than aspirin alone for protection against coronary events; and improved ability to distinguish the patients who initially respond to medical therapy who are at low risk for later severe angina from those at higher risk.

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We analyzed the clinical characteristics of 10 patients with pneumococcal endocarditis hospitalized between 1974 and 1984. Patients with pneumococcal endocarditis were typically middle-aged men. Forty percent were alcoholic. They sought medical attention early in the course of their illness and were given appropriate antibiotics promptly. The aortic valve was involved in seven patients. Five patients developed signs of severe valvular insufficiency, and congestive heart failure was present at the time of admission in four patients. Only three patients were recognized to have endocarditis prior to death or to the occurrence of a major complication of their infection. The total in-hospital mortality rate among these patients was 50%. Thus pneumococcal endocarditis is generally an acute, left-sided endocarditis that is associated with rapid valvular destruction and a high mortality rate. Unfortunately, recent advances in diagnosis and treatment of bacterial endocarditis have not substantially improved the outcome of this devastating infection.

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Unstable angina usually responds to medical management. Unfortunately, a third of patients with this condition may be expected to have severe angina in the ensuing year. We tested the ability of thallium 201 imaging with submaximal exercise to identify patients who have a poor clinical prognosis after an episode of unstable angina. In all, 37 patients were evaluated with (201)TI before hospital discharge and were assessed for severity of angina over the next 12 weeks. Of these, 20 had New York Heart Association class I or II angina during follow-up, 4 of whom had defects on (201)TI imaging that showed redistribution. In 17 patients class III or IV angina developed or they suffered an acute myocardial infarction after hospital discharge, and 15/17 had reversible defects on (201)TI imaging after submaximal stress (P<.001). (201)TI scintigraphy frequently identifies areas of ischemia with only submaximal exercise in patients whose unstable angina has responded to medical therapy.

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The volumes of the left ventricle (LV) and right ventricle (RV) were determined by scintigraphy, radiography, and weight, using hollow, morphologically accurate cardiac phantoms that ranged from 99-415 ml (RV) and 72-364 ml (LV). Self-attenuation within these simulated ventricles appeared negligible in view of the nearly linear correlation between scintigraphic and weight determined volumes. Scintigraphy compared favorably with radiography for estimating clinically encountered volumes of the RV and LV.

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We studied 30 consecutive patients with unstable angina during pain-free intervals with gated blood pool scintigraphy. The initial study was performed within 18 hours of admission to the coronary care unit. A second study was performed near the time of hospital discharge, after stabilization with medical therapy. Three months thereafter patients were categorized according to their worst anginal status following hospital discharge. Fifteen patients were New York Heart Association functional class I or II (group A); 15 patients were in functional class III or IV (group B). Left ventricular ejection fraction was similar at the time of initial study (55.9 +/- 2.18% and 56.0 +/- 3.55% for groups A and B respectively). At the time of hospital discharge the ejection fraction had risen to 60.3 +/- 1.85% (p less than 0.01) in group A and in group B it had fallen to 48.1 +/- 3.4% (p less than 0.005). End-systolic volume index in group B rose from 37 ml/m2 +/- 6.1 to 43 +/- 6.2 ml/m2 (p less than 0.005) at the time of the follow-up study. There were no significant intergroup patients during the two scintigraphic examinations. Eleven group B patients subsequently underwent coronary artery bypass surgery. A significant increase in ejection fraction and a significant decrease in end-systolic volume index were noted when these patients were restudied an average of 3.2 months after surgery. This study suggests that changes in left ventricular function during the course of unstable angina pectoris are common and may be detected by serial gated blood pool scintigraphy.(ABSTRACT TRUNCATED AT 250 WORDS)

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We conducted a multicenter, double-blind, placebo-controlled randomized trial of aspirin treatment (324 mg in buffered solution daily) for 12 weeks in 1266 men with unstable angina (625 taking aspirin and 641 placebo). The principal end points were death and acute myocardial infarction diagnosed by the presence of creatine kinase MB or pathologic Q-wave changes on electrocardiograms. The incidence of death or acute myocardial infarction was 51 per cent lower in the aspirin group than in the placebo group: 31 patients (5.0 per cent) as compared with 65 (10.1 per cent); P = 0.0005. Nonfatal acute myocardial infarction was 51 per cent lower in the aspirin group: 21 patients (3.4 per cent) as compared with 44 (6.9 per cent); P = 0.005. The reduction in mortality in the aspirin group was also 51 per cent--10 patients (1.6 per cent) as compared with 21 (3.3 per cent)--although it was not statistically significant; P = 0.054. There was no difference in gastrointestinal symptoms or evidence of blood loss between the treatment and control groups. Our data show that aspirin has a protective effect against acute myocardial infarction in men with unstable angina, and they suggest a similar effect on mortality.

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To determine the value of real-time, two-dimensional echocardiography (2-D echo) in unstable angina, regional wall motion on serial short-axis 2-D echo recordings was analyzed and summed segment scores of abnormal motion were compared and classified according to each patient's clinical status 12 weeks after hospital discharge. Nineteen male patients who fulfilled criteria for unstable angina and responded to medical therapy underwent 2-D echo study within 48 hours of admission and discharge. Of 11 patients with abnormal 2-D echo scores on admission, five patients had reduced scores and six patients had similar or increased scores at discharge. Six of eight patients who had scores of zero on admission had scores of zero at discharge. At follow-up, 11 patients had minimal or no angina pectoris (group 1), and eight patients had worsening angina or recurrent unstable angina (group 2). At discharge, 2-D echo studies showed that all group 1 patients had reduced or zero scores, while group 2 patients retained or increased their abnormal scores. This study shows that in patients with unstable angina, both transient and persistent abnormalities can be identified by 2-D echo. Abnormal segmental wall motion was transient or absent in patients with a good outcome, and worsened or remained abnormal in patients with a poor outcome.

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This study was undertaken to determine whether abnormalities on the echocardiograms of patients with unstable angina have any prognostic significance. 27 male patients, mean age 53 years, who fulfilled criteria for unstable angina and who responded to medical therapy, had echocardiograms within 48 h of admission and at discharge. Follow-up data were obtained from 7 patients during a postdischarge period of 6-26 weeks. 13 patients had mild exertional angina or were pain-free (group I) and 14 patients had either severe, stable angina pectoris or recurrence of their unstable angina (group II) during the follow-up period. When admission and discharge values were compared, the echocardiographic ratio of left ventricular end-diastolic dimension to mitral valve closure time (EDD/PR-AC) showed significant differences for both group I and group II (p less than 0.05). An abnormal EED/PR-AC ratio was present at discharge in 8 of 14 group II patients compared to only 1 of 13 group I patients (p less than 0.05). The mean values for end-diastolic dimension, mitral valve closure time, and amplitudes of interventricular septal and posterior left ventricular wall motion were not significantly different in comparisons between admission and discharge studies and between group I and group II patients. In 19 patients who had cardiac catheterization druing the follow-up period, the discharge EED/PR-AC ratio correlated inversely with the angiographic ejection fraction (r = 0.79; p less than 0.001).

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