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Two hundred patients with echocardiographically proven left ventricular hypertrophy underwent quantitative stress thallium tomography. The overall sensitivity and specificity were high (84% and 82%, respectively).

Among 23,059 patients who underwent exercise myocardial tomography between 1985 and 1994 at our institution, there were 817 (3.5%) with a strongly positive exercise electrocardiogram and normal myocardial tomograms. Among these, 52 patients had no conditions known to be associated with a false-positive exercise electrocardiogram and no previous coronary revascularization, and underwent coronary angiography. Of the 32 patients with significant coronary stenoses, 50% had 1-vessel disease and only 22% had 3-vessel disease (p < 0.05). Among 55 stenosed arteries, 56% were of moderate severity (50 to 74%), whereas only 9% had subtotal or total occlusion (95 to 100%) (p < 0.001). There was a significant gender difference in the prevalence of significant coronary stenoses (80% in male vs 24% in female patients, p < 0.0001). A strongly positive exercise electrocardiogram coupled with normal exercise myocardial tomograms is a rare clinical finding. In women, this finding is usually associated with normal coronary arteries, whereas in men it often denotes coronary artery disease, usually of mild to moderate degree.

Thallium-201 single photon emission computed tomography (SPECT) is superior to planar imaging for localizing native coronary stenoses, but has not yet been studied for assessing graft patency late after coronary artery bypass graft surgery (CABG). Accordingly, we studied 50 patients (40 males), aged 58 +/- 9 years (mean +/- SD), who presented for evaluation of angina (30 patients), atypical chest pain (20 patients), and other symptoms (9 patients), late after CABG (51 +/- 47 months). Patients with prior myocardial infarction were excluded. The mean ejection fraction was 58 +/- 17%. All patients underwent coronary angiography within 3 weeks of symptom-limited exercise thallium-201 SPECT. There were 119 grafts, of which 48 had > 50% stenosis by angiography. Thallium-201 SPECT detected 40 of these 48 (83%) stenosed grafts. The sensitivity of thallium-201 SPECT for detecting any graft stenosis was higher than that of the exercise electrocardiogram in patients with typical recurrent angina (84% vs 24%, p < 0.0001), as well as in those with atypical symptoms (70% vs 50%, p = 0.0039). The sensitivity of thallium-201 SPECT for correctly localizing the graft stenosis site was 82% for the left anterior descending, 92% for the right coronary, and 75% for the circumflex coronary artery. In conclusion, exercise thallium-201 SPECT is an excellent method to detect and localize graft stenosis late after CABG; it is far superior to the exercise electrocardiogram alone, both in patients with and without typical recurrent angina.

The purpose of this study was to define the reproducibility of sequential quantitative exercise thallium-201 tomography. This was an ancillary study of a randomized, double-blind, placebo-controlled trial evaluating the short-term efficacy of transdermal nitroglycerin patches in stable patients with angiographic coronary artery disease and no prior myocardial infarction. All 18 patients had a baseline tomographic perfusion defect involving > or = 5% of the left ventricle after treadmill exercise. At a minimum of 3 days (mean 6.1 +/- 1.8) after double-blind randomization to placebo, exercise thallium-201 tomography was repeated (study 2) using the same exercise protocol as in the baseline study (study 1). No significant differences in exercise parameters were observed from studies 1 to 2. Seventeen of 18 patients (94%) had an abnormal repeat exercise perfusion scan and 96% of initially abnormal vascular territories remained abnormal. The mean tomographic perfusion defect size was not significantly different from studies 1 (17.4 +/- 13.3%) to 2 (16.6 +/- 15.3%), nor were the components defined as scar and ischemia. A > or = 10% change in total perfusion defect size in an individual patient defined the 95% confidence interval for exceeding the variability of the tomographic technique. Quantitative exercise thallium-201 tomography is highly reproducible and can be used to accurately interpret temporal changes in myocardial perfusion in individual patients.

Amiodarone in doses of 200 to 400 mg/day has shown promise in secondary prevention trials for reducing mortality in patients surviving myocardial infarction who have complex ventricular ectopy or nonsustained ventricular tachycardia, or both. In an attempt to explore the lowest dose of amiodarone with antiarrhythmic and hemodynamic activity, we studied 48 patients (mean age 53 +/- 11 years, ejection fraction 23 +/- 9%, clinical heart failure in 85%) with nonsustained ventricular tachycardia. This was a 3-month, randomized, parallel, double-blind pilot study comparing placebo (n = 16) with amiodarone 50 mg/day (n = 15) and 100 mg/day (n = 17). Patients randomized to amiodarone received a mean loading dose of 422 mg/day for the first study week. At the end of the 12 weeks, amiodarone (100 mg) significantly reduced ventricular premature complexes (177 +/- 64 to 98 +/- 38/hour), couplets (8 +/- 3 to 4 +/- 2/hour), and runs of nonsustained ventricular tachycardia (13 +/- 7 to 3 +/- 2/day), all p < 0.01 versus baseline. In addition, 10 of 14 patients taking 100 mg/day had total suppression of nonsustained ventricular tachycardia compared with 4 of 15 taking placebo, p = 0.021. Left ventricular ejection fraction improved by > or = 7% (absolute) in 11 of 29 patients taking amiodarone as compared with only 1 of 15 placebo patients (p = 0.02). In these 11 patients with the greatest measurable hemodynamic improvement, amiodarone significantly increased ejection fraction (21 +/- 7% to 33 +/- 11%, p < 0.01), stroke volume index (28 +/- 9 to 40 +/- 7 ml/m2, p < 0.01) and decreased end-systolic volume index (116 +/- 48 to 92 +/- 44 ml/m2, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

The diagnostic accuracy, safety and tolerance of adenosine thallium scintigraphy have been reported using a 2-site intravenous infusion with either a titrated or fixed-dose protocol. A single-site infusion would considerably simplify the test procedure, but its safety must be established before it can be recommended. Accordingly, 400 consecutive patients who had adenosine and thallium-201 administered through the same intravenous line were classified into 2 groups. Group I (n = 201) patients received a 7-minute titrated intravenous infusion of adenosine, with an initial dose of 50 micrograms/kg/min that increased at 1-minute intervals to a maximum of 140 micrograms/kg/min. Group II (n = 199) patients received a fixed dose of adenosine at 140 micrograms/kg/min for 6 minutes. Adenosine significantly (p < 0.001) increased heart rate and decreased systolic blood pressure by similar amounts in both groups. Adverse effects occurred more often (88 vs 71%, p < 0.001) and started earlier (2.8 vs 3.6 minutes, p < 0.001) in group II. There was no significant difference in the occurrence of second- and third-degree atrioventricular block between the 2 groups (4.0 vs 5.0%); however, chest pain, flushing and nausea were all more frequent in group II. Severe side effects were seldom seen in either group and occurred in 9 group I and 8 group II patients. Scintigraphic findings were similar in both groups. Transient perfusion defects were seen more often in patients with than without second- or third-degree atrioventricular block (42 vs 21%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Twelve patients with exercise-induced ST-segment elevation without prior myocardial infarction, electrocardiographic evidence of left ventricular hypertrophy or left bundle branch block underwent thallium-201 tomography immediately after exercise and 4 hours later. Coronary angiography and left ventriculography were performed within an average of 8 days of exercise testing. Five patients had repeat exercise thallium-201 tomography after medical therapy or revascularization. All patients had large, reversible perfusion defects (average defect size 33.5 +/- 13%), with 11 of 12 patients having a > or = 25% stress perfusion defect. In 10 patients with atherosclerotic coronary artery disease, the average stenosis of the involved vessel was 93 +/- 9% (range 70 to 100). The electrocardiographic leads with ST-segment elevation predicted the site of reversible hypoperfusion. Two patients had extensive, reversible anterior hypoperfusion due to exercise-induced spasm of minimally stenosed left anterior descending coronary arteries. Follow-up exercise testing in 5 patients showed abolition of reversible hypoperfusion and ST changes after medical therapy or revascularization. In patients without prior myocardial infarction, exercise-induced ST-segment elevation signifies extensive, reversible hypoperfusion that can be abolished by revascularization in patients with critical coronary stenoses and by medical therapy in those with coronary vasospasm.

Of all currently available techniques, thallium-201 single-photon emission computed tomography (SPECT) is the most time-tested noninvasive method for the detection of coronary artery disease (CAD). Recent pooled data show an overall sensitivity of 90% and a specificity of 70% for thallium-201 SPECT. Of patients with single-vessel coronary disease, 83% are identified by SPECT. Nearly all patients with double- and triple-vessel coronary disease (93% and 95%, respectively) are also identified. Thallium-201 SPECT imaging is also very effective in diagnosing CAD imaging is also very effective in diagnosing CAD using pharmacologic stress testing. In certain patient populations (e.g., in sedentary patients or those using anti-ischemic medications), pharmacologic stress testing with dipyridamole or adenosine may be a logical alternative to exercise testing. Moreover, many patients have physical disabilities that preclude appropriate exercise testing. Intravenous adenosine is a very potent direct coronary vasodilator, with the advantage of an ultrashort half-life, which eliminates the need to administer an antagonist in the majority of patients. In addition, the dosage of adenosine can be adjusted during the infusion, if necessary. The importance of thallium-201 SPECT during exercise or pharmacologic vasodilation transcends diagnosis, since it also plays an important role in the prognostic evaluation of patients with stable angina or postmyocardial infarction. Risk evaluation can be done with submaximal exercise electrocardiographic testing, but there is evidence that the addition of perfusion scintigraphy enhances the ability to predict future risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Pharmacologic coronary vasodilation as an adjunct to thallium-201 myocardial perfusion scintigraphy provides an important alternative form of stress that has been increasingly used in patients unable to perform an exercise stress test. Although dipyridamole has traditionally been used for this purpose, there are several compelling reasons why adenosine may be a preferable agent. First, dipyridamole acts by blocking the reuptake and transport of adenosine, which is the effective substance responsible for coronary vasodilation. Second, exogenous adenosine has a very short half-life (less than 2 seconds), which explains its very short duration of action as well as the brief, self-limiting duration of its side effects. Third, the adenosine infusion is controllable and may be increased or decreased as desired. Fourth, the coronary vasodilation induced by the doses of adenosine we recommend (140 micrograms/kg/min) may be more profound than that induced by the standard dipyridamole dose. Our experience to date, with nearly 1,000 patients studied, shows the adenosine thallium-201 test to be practical and well tolerated, with high sensitivity (87%) and specificity (94%) for detecting coronary artery disease.

Exercise thallium-201 perfusion scintigraphy has been used extensively over the last decade for the detection and localization of coronary artery disease. Single-photon emission computed tomography (SPECT) is a refinement of presently available techniques, offering improved identification over planar imaging of individual vessel stenosis and quantification of the extent of abnormally perfused myocardium. In this review, the planar and SPECT techniques are discussed in light of the most recently published large patient series, and with regard to the many factors that affect the sensitivity and specificity of perfusion imaging in identifying coronary artery disease. The clinical implications of exercise perfusion scintigraphy and its future applications in cardiology practice are discussed.

The mechanisms responsible for inhomogeneous myocardial blood flow after oral administration of a large dose (300 mg) of dipyridamole were assessed in 27 patients with serial thallium-201 single-photon emission computed tomography (SPECT) and simultaneous 2-dimensional echocardiograms. Myocardial tomographic images were obtained 50 minutes and 3 to 4 hours after administration of dipyridamole. Two-dimensional echocardiograms were recorded at baseline and then every 15 minutes for 60 minutes. Dipyridamole caused only a mild reduction in blood pressure (from 129 +/- 18 to 126 +/- 16 mm Hg) and a mild increase in heart rate (from 69 +/- 15 to 73 +/- 4 beats/min). Sixteen patients had perfusion defects after dipyridamole by SPECT, which underwent partial or total filling-in. Fourteen of these patients (87.5%) had either a new abnormality or further deterioration of a preexisting wall motion abnormality by 2-dimensional echocardiography, and thus were considered to have developed transient ischemia during dipyridamole administration. Ten of 11 patients (91%) with normal perfusion or fixed defects by SPECT had no further deterioration in wall motion after oral dipyridamole, and were thus considered to have no evidence of myocardial ischemia. In conclusion, most patients with transient thallium-201 defects after dipyridamole develop transient worsening of resting wall motion by 2-dimensional echocardiography, suggestive of true myocardial ischemia. Because myocardial oxygen demand, as indicated by the heart rate-blood pressure product, did not change significantly, the mechanism of myocardial ischemia in these patients is likely to be diminished regional blood flow related to a "subendocardial steal" induced by dipyridamole.

Beta-adrenergic blocking agents may have negative inotropic effects that are particularly worrisome in patients with depressed cardiac function. Their membrane-stabilizing properties may be a contributing factor. Sotalol is currently thought not to cause significant myocardial depression. Intravenous sotalol administration has minimal effects on resting stroke volume, although heart rate and consequently cardiac output are significantly decreased. Systolic blood pressure decreases, with a minimal change in diastolic or mean pressure. Hemodynamic effects are usually seen within 15 to 20 minutes of administration. Hemodynamic indexes are maintained even in patients with mildly depressed ejection fractions (mean ejection fraction of 43 +/- 15%) after oral sotalol administration. Although heart rate decreases, cardiac index is unchanged because of a significant increase in stroke volume index. The latter results from an increase in preload (secondary to bradycardia) and a decrease in afterload. Sotalol is well tolerated, although occasionally it may cause worsening heart failure. This is seen in patients with markedly depressed left ventricular function and inadequate cardiac reserve characterized by an inability to increase stroke volume and cardiac output with exercise. Long-term (1-year) patient follow-up reveals no significant hemodynamic deterioration from initial values obtained after oral administration.

Mitral valve motion, left ventricular segmental contraction and severity of arterial stenosis were analyzed in 92 patients with coronary artery disease and 28 patients with "atypical chest pain" and normal coronary arterio-rams. Mitral valve motion was evaluated for the presence or absence of leaflet prolapse. Segmental contraction was evaluated by calculating the percent shortening of six chords of the left ventricle measured from right anterior oblique ventriculograms. The severity of disease in each coronary vessel (left anterior descending, left circumflex and right coronary) was graded on a scale of 1 (0 to 30 percent stenosis) to 5 (complete occlusion). Mitral valve prolapse was not suspected clinically but observed angiographically in 15 of 92 patients with coronary artery disease and in 5 of 28 patients with normal coronary arteriograms. In nine patients with coronary artery disease, the prolapse was restricted to the posterior leaflet, in five it was in both the anterior and the posterior leaflets and in one patient in the anterior leaflet only. Mitral regurgitation was noted in seven patients with coronary artery disease; it was mild in six and moderate in one. Among the patients with coronary artery disease, 12 of the 15 (80 percent) with mitral valve prolapse had left ventricular asynergy compared with 63 of the 77 (82 percent) without valve prolapse. The mean scores for severity of disease in the left anterior descending, circumflex and right coronary arteries were, respectively, 4.2, 2.5 and 3.2 in the patients with valve prolapse and 4.2, 2.2 and 3.5 in those without prolapse. In summary, there was no significant correlation between mitral valve prolapse and distribution of coronary arterial obstructions or abnormal patterns of left ventricular segmental contraction. There was a high frequency of mitral valve prolapse in patients with severe coronary artery disease and in those with normal coronary arteriograms and atypical chest pain.

Coronary arteriovenous fistula is a rare cause of congestive heart failure in the newborn. We describe a 2 day old infant with a large fistula between the right coronary artery and right ventricle that caused fatal congestive heart failure. An echocardiographic study revealed a large right ventricle, paradoxical motion of the interventicular septum and an enlarged aorta, suggesting an unusual location of a left to right shunt. The diagnosis was established at cardiac catheterization when a large left to right shunt was found at the ventricular level; the fistula was visualized by angiography.

To determine the effects of exercise training on left ventricular performance and myocardial perfusion in coronary artery disease, rest and exercise radionuclide angiocardiography and thallium-201 scintigraphy were performed before and after 12 weeks of training in 16 coronary patients. After training, 15 of the 16 patients had improved exercise tolerance; total treadmill exercise duration increased from (mean +/- standard error of the mean) 491 +/- 37 to 602 +/- 31 seconds (p less than 0.01), and the estimated rate of oxygen consumption (VO2 max) increased from 29.4 +/- 1.4 to 33.8 +/- 1.2 ml/kg per min (p less than 0.001). Resting left ventricular ejection fraction increased from 52 +/- 4 to 57 +/- 4 percent (p less than 0.02); no change occurred in left ventricular functional reserve assessed by ejection fraction and regional wall motion response to exercise at the same rate-pressure product before and after training. Myocardial perfusion at equivalent pre- and post-training cardiac work loads during exercise and on redistribution was unchanged by training. It is concluded that in patients with coronary heart disease, physical training increases exercise tolerance, and results in minimal improvement in resting left ventricular systolic performance. Functional reserve of both left ventricular systolic performance and the coronary circulation appears to be unchanged by exercise training. These data suggest that the beneficial effects of training for 12 weeks in patients with coronary artery disease predominantly result from factors other than improvement in left ventricular pump performance or perfusion.

Exercise-induced coronary arterial spasm is an infrequently recognized phemonemon whose mechanism and management are not well established. In two patients with reproducible exercise-induced S-T segment elevation and angina pectoris thallium-201 scintigraphy showed areas of reversible anteroapical hypoperfusion, and gated radionuclide ventriculography revealed anteroapical hypokinesia with a decrease in left ventricular ejection fraction at peak exercise. During coronary arteriography supine exercise provoked occlusive spasm of the left anterior descending coronary artery, which at rest had only minimal plaques. Consequently, treadmill testing was performed with five different pharmacologically provoked interventions: direct vasodilatation (nitrates), alpha adrenergic blockade (phenmoxybenzamine), beta adrenergic blockade (propranolol), calcium flux blockade (verapamil), and prostaglandin inhibition (indomethacin). Exercise-induced coronary arterial spasm, manifested as S-T segment elevation and angina, was prevented by nitrates, but was not eliminated by short-term oral administration of an alpha or beta blocking agent, a calcium antagonist or a prostaglandin inhibitor. Further, beta adrenergic blockade appeared to be detrimental. Thus, this study demonstrates (1) that coronary arterial spasm may be the underlying mechanism of at least some cases of exertional angina associated with transient perfusion deficits and left ventricular dysfunction, and (2) that it may be prevented by oral nitrates.

To assess the effects of nifedipine on left ventricular function and regional myocardial perfusion, exercise radionuclide ventriculography was performed in 15 men (median age 59 years) and exercise thallium-201 scintigraphy was done in 11 of them, before and 90 minutes after the oral administration of 20 mg of nifedipine. All patients had stable angina and angiographically proved coronary artery disease without evidence of spasm. Exercise tolerance after administration of nifedipine increased from 343 +/- 42 seconds to 471 +/- 50 seconds (p less than 0.01), whereas the peak exercise double product remained essentially unchanged (difference not significant). Ejection fraction improved significantly at rest (from 49 +/- 3.6% to 52 +/- 3.3%, p less than 0.05) and at peak exercise (42 +/0 3.3% to 47 +/- 3.7%, p less than 0.05). Nifedipine also resulted in an improved segmental wall motion score (4.3 +/- 2.3 to 3.0 +/- 2.3, p less than 0.05; 0 = normal and 4 = worst degree of dysfunction). The ejection fraction increased by more than 5% in one third of the patients at rest, and in more than half of the patients at peak exercise. Improved exercise myocardial perfusion occurred in 5 of 11 patients (45%) and in 7 of 28 segments (25%) with reversible hypoperfusion. Thus, nifedipine produces significant improvement in global and regional left ventricular function in patients with coronary artery disease and stable angina. This may be accounted for, at least in part, by improvement in myocardial perfusion.

A prospective, randomized trial was designed to assess the efficacy of intracoronary thrombolytic therapy with streptokinase (STK) in acute myocardial infarction. Sixty-four patients with acute myocardial infarction were randomized within 6 hours of onset of symptoms to 1 of 3 groups. Sixteen patients were treated by conventional means (control group). Nineteen patients underwent coronary arteriography and received corticosteroids and intracoronary and intravenous nitroglycerin (NTG group). Twenty-nine patients received management identical to that of the NTG group, with the addition of intracoronary STK therapy (STK group). Recanalization was demonstrated in 21 of 29 patients (72%) in the STK group. Global and regional ejection fraction (EF) was determined by radionuclide ventriculography before any intervention and 7 to 10 days later. No significant improvement in global EF was achieved in the control and NTG groups. In STK patients as a group, global EF did not increase significantly; however, in patients recanalized with STK, EF improved from 42 +/- 17% to 49 +/- 16% (p = 0.023). All groups showed wide variability of response. Improvement in global EF of more than 5% was noted in 44% of patients recanalized with STK. When subgrouped on the basis of initial global EF of 45% or less or more than 45%, only patients recanalized with STK with an initial EF of 45% or less had an improved global EF (from 30 +/- 10% to 42 +/- 10%, p = 0.015).(ABSTRACT TRUNCATED AT 250 WORDS)

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.