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Nuclear cardiology has made significant advances since the first reports of planar scintigraphy for the evaluation of left ventricular perfusion and function. While the current “state of the art” of gated myocardial perfusion single-photon emission computed tomographic (SPECT) imaging offers invaluable diagnostic and prognostic information for the evaluation of patients with suspected or known coronary artery disease (CAD), advances in the cellular and molecular biology of the cardiovascular system have helped to usher in a new modality in nuclear cardiology, namely, molecular imaging. In this review, we will discuss the current state of the art in nuclear cardiology, which includes SPECT and positron emission tomographic evaluation of myocardial perfusion, evaluation of left ventricular function by gated myocardial perfusion SPECT and gated blood pool SPECT, and the evaluation of myocardial viability with PET and SPECT methods. In addition, we will discuss the future of nuclear cardiology and the role that molecular imaging will play in the early detection of CAD at the level of the vulnerable plaque, the evaluation of cardiac remodeling, and monitoring of important new therapies including gene therapy and stem cell therapy.

The hallmark of endothelial activation, an early and critical step in many alloimmune and inflammatory responses, is the transcriptional induction and expression of endothelial adhesion molecules (eg, vascular cell adhesion molecule-1 [VCAM-1]). We assessed the feasibility of VCAM-1-targeted in vivo detection of endothelial activation using I-125-labeled-F(ab')2 fragments of E1/6, a monoclonal antibody against human but not murine VCAM-1. The Kd and Bmax, determined by saturation binding in tumor necrosis factor (TNF)-activated human endothelial cells (ECs), were 3.2 +/- 0.6 nmol/L and 5600 +/- 300 binding sites per EC, respectively. Biodistribution and in vivo binding characteristics of I-125-E1/6 F(ab')2 were assessed in a novel chimeric human/mouse model, in which human skin (as a source of human microvasculature) is grafted onto SCID/beige mice. I-125-E1/6 F(ab')2 localized to TNF-activated human skin grafts as detected by autoradiography and gamma well-counting. Relative uptakes (uptake in human skin graft/uptake in the surrounding mouse skin) were, respectively, 2.6 +/- 0.8 (n = 14) and 1.6 +/- 0.3 (n = 12) for E1/6 and MOPC-21, an isotype-matched control antibody (P < .01). The preferential uptake in human skin graft was not due to differences in tissue vascularity assessed by Tc-99m-labeled murine red blood cells. In conclusion, the chimeric human/mouse model is a novel experimental tool for in vivo evaluation of human endothelial cell-specific radiopharmaceuticals. Although I-125-E1/6 F(ab')2 localized to human skin grafts, the limited number of VCAM-1 molecules/endothelial cell adversely affects its suitability as a target for in vivo imaging of endothelial activation.

In this issue of iJACC (JACC: Cardiovascular Imaging) , Botvinick et al. ([1][1]) perform a complex study involving the performance of equilibrium radionuclide myocardiography with phase analysis during ventricular tachycardia. The authors identify specific characteristics that define tolerability

Objectives. We sought to investigate the mechanism of a mental stress–induced fall in left ventricular ejection fraction (LVEF) in patients with coronary artery disease. Background. Mental stress induces a fall in LVEF in a significant proportion of patients with coronary artery disease. This is accompanied by an increase in heart rate, blood pressure and rate–pressure product. Whether the mental stress–induced fall in LVEF is due to myocardial ischemia, altered loading conditions or a combination of both is not clear. Methods. Left ventricular (LV) function was studied noninvasively by serial equilibrium radionuclide angiocardiography and simultaneous measurement of peak power, a relatively afterload-independent index of LV contractility, in 21 patients with coronary artery disease (17 men, 4 women) and 9 normal subjects (6 men, 3 women) at baseline, during mental stress and during exercise. Peripheral vascular resistance (PVR), cardiac output (CO), arterial and end-systolic ventricular elastance (Ea, Ees) and ventriculoarterial coupling (V/AC) were also calculated. Patients underwent two types of mental stress—mental arithmetic and anger recall—as well as symptom-limited semisupine bicycle exercise. Results. Nine patients (43%) had an absolute fall in LVEF of ≥5% (Group I) in response to at least one of the mental stressors, whereas the remaining patients did not (Group II). Group I and Group II patients were similar in terms of baseline characteristics. Both groups showed a significant but comparable increase in systolic blood pressure (15 ± 7 vs. 9 ± 10 mm Hg, p = 0.12) and a slight increase in heart rate (7 ± 4 vs. 8 ± 7 beats/min, p = 0.6) and a comparable increase in rate–presure product (2.2 ± 0.9 vs. 1.9 ± 1.2 beats/min × mm Hg, p = 0.6) with mental stress. However, PVR increased in Group I and decreased in Group II (252 ± 205 vs. −42 ± 230 dynes·s·cm−5, p = 0.006), and CO decreased in Group I and increased in Group II (−0.2 ± 0.4 vs. 0.6 ± 0.7 liters/min, p = 0.02) with mental stress. There was no difference in the change in peak power (p = 0.4) with mental stress. With exercise, an increase in systolic blood pressure, heart rate, rate–pressure product and CO and a fall in PVR were similar in both groups. Of the two mental stressors, anger recall resulted in a greater fall in LVEF and a greater increase in diastolic blood pressure. Exercise resulted in a fall in LVEF in 7 patients (33%). However, exercise-induced changes in LVEF and hemodynamic variables were not predictive of mental stress–induced changes in LVEF and hemodynamic variables. Conclusions. Abnormal PVR and Earesponses to mental stress and exercise are observed in patients with a mental stress–induced fall in LVEF. Peripheral vasoconstrictive responses to mental stress contribute significantly toward a mental stress–induced fall in LVEF.

Current protocols for use of tissue-type plasminogen activator in acute myocardial infarction include heparin estimated by the activated partial thromboplastin time (aPTT). Recent reports indicate a risk of recurrent ischemic events with long aPTT values. Longer aPTT values in the Thrombolysis in Myocardial Infarction-II (TIMI II) Trial, obtained within the first 48 hours, were associated with patency at 18 to 48 hours and better left ventricular function at discharge (average 9.6 days), but also with emergency catheterizations within the first 48 hours and, weakly, with recurrent ischemia during the first 18 hours. A moderate decrease in fibrinogen, compared with a “small” decrease, was also associated with patency, but a “large” decrease was associated with hemorrhagic events. Patency was associated with higher fibrinogen values and higher plasminogen values at baseline. The aPTT results support frequent monitoring during the first 24 to 48 hours to ensure optimal clinical outcome. The coagulation factor results suggest that there may be an optimum window for fibrinogenolysis in this setting. (Am Heart J 1998;135:29-37.)

This study sought to determine the significance of abnormal thallium-201 (Tl-201) lung uptake on stress imaging in the absence of perfusion abnormalities.Abnormal Tl-201 lung uptake, represented by an increased lung/heart ratio (LHR), on stress imaging is a marker of stress-induced left ventricular dysfunction and poor prognosis in patients with coronary artery disease.We evaluate 1,271 patients from the Thrombolysis in Myocardial Infarction (TIMI)-IIIB trial (86% of TIMI-IIIB cohort) with unstable angina or non-Q wave myocardial infarction, who underwent predischarge exercise (92%) or dipyridamole stress (8%) Tl-201 imaging. An increased LHR (or = 0.50) was related to perfusion abnormalities and adverse cardiac events at 1 year.Of 1,271 patients, there were 762 (60%) with and 509 (40%) without perfusion abnormalities. An increased LHR was seen in 227 patients (18%) (173 [23%] with, 54 [11%] without perfusion abnormalities). Patients with an increased LHR had a lower left ventricular ejection fraction, higher body weight, lower exercise capacity and a higher prevalence of angina on exercise than patients with a normal LHR. In the two groups with increased LHR, there was no difference in age, hypertension, previous myocardial infarction, total exercise time, frequency of angina and ST segment depression on exercise. However, the group with an increased LHR and normal myocardial perfusion had a preponderance of women (65% vs. 30%, p0.001). At 1-year follow-up, patients with an increased LHR had a higher cardiac event rate than those with a normal LHR (18% vs. 10%, respectively, p = 0.001) despite a higher revascularization rate (28% vs. 15%, p0.001). An increased LHR was associated with increased adverse cardiac events, irrespective of the presence or absence of perfusion abnormalities.An increased LHR continues to be associated with higher adverse cardiac events in the current era of aggressive interventional management of coronary artery disease. An increased LHR in the absence of myocardial perfusion abnormality is seen mostly in women and overweight patients. However, despite the apparent absence of perfusion abnormalities, an increased LHR in this group is also associated with a higher rate of adverse cardiac events.

Previous studies have shown an association between distortion of the terminal portion of the QRS (QRS[+] pattern: emergence of the J point ≥50% of the R wave in leads with qR configuration, or disappearance of the S wave in leads with an Rs configuration) on admission and in-hospital mortality in acute myocardial infarction (AMI). However, the mechanism for this association is not known. We assessed the relation between QRS(+) pattern and coronary angiographic findings, infarct size, and long-term prognosis in the Thrombolysis In Myocardial Infarction 4 trial. Patients were allocated into 2 groups based on the presence (QRS[+], n = 85) or absence (QRS[−], n = 293) of QRS distortion. The QRS(+) patients were older (mean ± SD: 61.1 ± 10.6 vs 57.5 ± 10.6 years, p = 0.004), had more anterior AMI (49% vs 37%, p = 0.04), and less previous angina (42% vs 54%, p = 0.05). QRS(+) patients had larger infarct size as assessed by creatine kinase release over 24 hours (209 ± 147 vs 155 ± 129, p = 0.003), and predischarge sestamibi (MIBI) defect (17.9 ± 15.9% vs 11.2 ± 13.4%, p

Thirty patients with stable angina pectoris and ischemia on stress perfusion imaging underwent continuous ambulatory left ventricular (LV) function monitoring. Mental stress was induced by mental arithmetic. Fifteen patients developed transient LV dysfunction during mental arithmetic. Patients were followed for 2 years for adverse cardiac events. Twelve patients had cardiac events over 1 year (myocardial infarction in 4, and unstable angina in 8). Nine of 15 patients (60%) with and only 3 of 15 (20%) without mental stress-induced LV dysfunction developed cardiac events (p = 0.025). A higher proportion of patients with cardiac events were taking beta blockers (p = 0.01) and had lower resting heart rates (p = 0.002) than those without cardiac events. There was no difference in the baseline characteristics between the groups of patients with and without cardiac events. At 2-year follow-up, 10 of 15 patients (67%) with mental stress-induced LV dysfunction had adverse events compared with only 4 of 15 (27%) with no mental stress-induced LV dysfunction (p = 0.025). Thus, in this cohort of patients with stable angina pectoris, mental stress-induced LV dysfunction was associated with higher cardiac events on follow-up. The exact mechanism of this association is not clear. Mental stress may be a trigger for adverse cardiac events in these patients. Transient LV dysfunction in response to mental stress may be a marker of abnormal cardiovascular reactivity to emotional and psychological stimuli in patients with coronary artery disease and may be useful for risk stratification.

Regional and global left ventricular dysfunction caused by coronary artery disease may be reversible in a significant proportion of cases. This fact has important clinical implications. The choice of the optimal nuclear imaging technique for the detection of myocardial viability is a matter of ongoing debate. Currently the choice of technique depends on the clinical question to be answered, the local availability of the technique, and local expertise. Cost considerations may also play an important role in choice of technique.

To ascertain whether the outcome of patients with suspected myocardial infarction differs when chest pain is still present at initiation of thrombolytic therapy, participants in the Thrombolysis in Myocardial Infarction Phase II study, all of whom presented within 4 hours of symptoms onset, were retrospectively divided into 2 groups: (1) those with chest pain present at onset of intravenous thrombolysis, n = 3,000; and (2) those who were free of chest pain on beginning intravenous thrombolytic therapy, n = 337. Patients free of chest pain were older (58 vs 57 years, p = 0.01), more often women (23 vs 17%, p = 0.01), had fewer electrocardiographic leads with ST elevation (3.8 vs 4.1, p 0.55 (35 vs 31%, p = 0.001) and fewer developed congestive heart failure (12 vs 20%). At 1-year follow-up, fewer pain-free patients developed congestive heart failure (15 vs 21%, p = 0.009), but no differences existed between the 2 groups in frequency of death, reinfarction, coronary angioplasty, bypass surgery or anginal class. Thus, there are several observations in patients who were free of chest pain at onset of lytic therapy. (1) The majority developed enzymatic or electrocardiographic evidence of acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Objectives. The present study evaluated our experience with coronary artery bypass grafting in patients with severe left ventricular dysfunction.Background. Despite the ominous prognosis of advanced ischemic cardiomyopathy, coronary artery bypass grafting in this setting remains controversial because of concerns over operative risk and lack of functional or survival benefit.Methods. We analyzed the data of 83 consecutive patients (69 men, 14 women, aged 42 to 83 years [mean 66.8]) with a left ventricular ejection fraction ≤30% who underwent isolated coronary artery bypass grafting (withoot aneurysmectomy, valve replacement or other open heart procedures) performed by one surgeon during a 6-year period. The ejection fraction ranged from 10% to 30% (mean 24.6%). Preoperatively, 49% of patients had angina, 52% had congestive heart failure (17% with pulmonary edema) and 30% manifested significant ventricular arrhythmia. The mean number of grafts was 2.7/patient. The internal mammary artery was used in 82% of grafts to the left anterior descending coronary artery. The intraaortic balloon pump was required therapeutically (for angina or pump failure) in 19% of patients and was prophylactically placed preoperatively in another 43% of patients.Results. The hospital mortality rate was 8.4% (7 of 83). The mortality rate was 3.3% (2 of 61) in those patients who did not require admission to an intensive care unit immediately before operation. Canadian Cardiovascular Society angina class improved postoperatively by 1.9 categories and New York Heart Association congestive heart failure class by 1 category. Left ventricular ejection fraction (assessed postoperatively in 68 of 76 hospital survivors) improved from 24.6% preoperatively to 33.2% postoperatively (36% increase) (p < 0.001). At 1 and 3 years, respectively, all-cause survival was 87% and 80% and freedom from cardiac death was 89.8% and 84.5%.Conclusions. In patients with coronary artery disease and advanced ventricular dysfunction: 1) coronary artery bypass grafting can be performed relatively safely, 2) good medium-term survival is attained, 3) improvement in left ventricular function can be documented objectively after bypass grafting, 4) quality of life is improved (as reflected by improvement in anginal and congestive heart failure status), and 5) the internal mammary artery can safely be used as a conduit. The use of coronary artery bypass grafting is encouraged for this group of patients and may provide a viable alternative to transplantation in selected patients.

Objectives. We examined the relationship of the psychological profile to left ventricular dysfunction induced during mental stress.Background. The contribution of psychological factors to mental stress-provoked silent myocardial ischemia has not been explored.Methods. Thirty patients with chronic stable coronary artery disease and a reversible defect on stress thallium-201 imaging completed a psychological assessment by questionnaire and Structured Interview, serially administered mental stress and brief walking exercise. Blood pressure, electrocardiogram (ECG) and left ventricular indexes were obtained by ambulatory serial radionuclide ventriculography. Silent ventricular dysfunction was defined by a decrease ≥0.05 in ejection fraction or ≥1 mm in ST segment on the ECG in the absence of symptoms.Results. Of the 30 patients, 15 (Group I) had evidence of silent left ventricular dysfunction during mental arithmetic. The other 15 (Group II) showed no change. In addition, 18 of 30 patients had this dysfunction during the Structured Interview. Both ischemic and nonischemic groups developed comparable and significant increases in heart rate and blood pressure. Group I patients were distinguished by higher scores on measures of aggressive responding (p < 0.001), trait anger (p < 0.0001), hostile affect (p < 0.003) and an index of behavioral reactivity (p < 0.003) and a lower score on anger control (p < 0.001). No other variables, including historical and clinical indexes, discriminated between the two groups.Conclusions. Patients with coronary artery disease and mental stress-provoked silent ventricular dysfunction were distinguished by a psychological profile consistent with emotional reactivity to social interaction and mental provocation, with anger as the predominant affective state. Patients with such a profile may be at risk of frequent silent left ventricular dysfunction.

To determine the effect of thrombolytic therapy on the frequency of right ventricular (RV) dysfunction, and whether RV dysfunction is a risk factor for morbidity and mortality after discharge from the hospital, 1,110 patients in the Thrombolysis in Myocardial Infarction (TIMI) II trial with acute inferior wall left ventricular myocardial infarction were studied. RV dysfunction was defined as an RV wall motion abnormality on equilibrium radionuclide ventriculography performed a mean of 9 days after admission to the hospital. Fifty-eight patients (5%) had RV dysfunction. Baseline clinical characteristics among patients with and without RV dysfunction were similar. However, patients with RV dysfunction had a lower mean left ventricular ejection fraction (51.2 +/- 1.2% vs 55.5 +/- 0.3%; p < 0.001) and a greater frequency of in-hospital complications. Angiographic data from patients undergoing protocol catheterization 18 to 48 hours after hospital admission show that the infarct-related artery was more likely to be occluded in those with RV dysfunction (48% [15 of 31] vs 14% [68 of 495]; p < 0.001). There was no difference in the frequency of multivessel disease between the 2 groups. In patients with RV dysfunction in whom radionuclide ventriculography was repeated 6 weeks after hospital discharge, RV wall motion abnormalities persisted in only 18% (8 of 45). Mortality in the year after discharge was 3.5% (2 of 58) among patients with RV dysfunction compared with 1.7% (18 of 1,052; p = NS) among those without RV dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Congestive heart failure (CHF) is typically associated with impaired left ventricular (LV) systolic performance. Few reports exist describing the long-term outcome in patients with CHF and normal LV systolic function. Fifty-two patients initially hospitalized with CHF and intact LV function (ejection fraction greater than or equal to 45%) were followed for 7 years. Mean age when initially identified was 71 +/- 11 years (range 36 to 96), and average LV ejection fraction was 61 +/- 11%. CHF was graded by a clinicoradiographic index, with a mean of 7.0 +/- 2.3 (range 3 to 12, 13 indicates worst CHF). A third heart sound was present in 19 patients (37%), and 17 (33%) had presented with acute pulmonary edema. Principal cardiovascular diagnoses were coronary artery disease in 27 (52%), hypertensive heart disease in 16 (31%) and restrictive cardiomyopathy in 7 (13%). At 7 years, cardiovascular mortality was 46% (24 of 52), and noncardiovascular mortality was 10% (5 of 52). Survival was not correlated with age, principal diagnosis, third heart sound, pulmonary edema at presentation, LV ejection fraction, or presence or degree of LV diastolic dysfunction. Cardiovascular morbidity, consisting of nonfatal recurrent CHF, myocardial infarction, unstable angina or other cardiovascular events occurred in 29% (15 of 52). Combined cardiovascular mortality and morbidity was 75% (39 of 52). In patients with CHF, intact LV systolic function does not confer the same favorable prognosis it defines in other clinical situations. For such patients, the risk of future cardiovascular events is high, a finding that should be considered when designing therapeutic strategies in this group.

Nuclear imaging techniques are useful in studying right ventricular size, contractility, regional wall motion, and ejection fraction. These studies can be used to obtain relevant information about right ventricular function in various cardiopulmonary diseases.

The ability of technetium (Tc)-99m sestamibi myocardial perfusion imaging at rest to evaluate myocardial infarction and first-pass ejection fraction was studied in a trial involving 18 institutions. Protocol I compared regional perfusion with occurrence of infarction by Q wave or by gated blood pool scan wall motion abnormality in 146 patients. Protocol II assessed first-pass right and left ventricular ejection fraction in 85 patients. In protocol I, Tc-99m sestamibi images were abnormal in 104 of 111 patients (94%) with both a Q wave and a gated scan wall motion abnormality and was normal in 23 of 25 patients (92%) in whom both were normal. Therefore, concordance existed in 105 (94%) patients. Of 115 patients with a Q wave, 107 (93%) had an abnormal Tc-99m sestamibi study. Of 115 patients with a gated scan wall motion abnormality, 108 (94%) had an abnormal Tc-99m sestamibi study. Tc-99m sestamibi imaging showed corresponding perfusion abnormalities in 81% of 69 anterior Q-wave infarcts, 73% of 55 inferior Q-wave infarcts and 88% of 8 posterior infarcts. Specificity in normal regions on electrocardiography and wall motion was 91, 100 and 100%, respectively, for anterior, inferior and posterior regions, respectively, between wall motion and perfusion. Of 17 myocardial segments per patient, there was concordance in 74% of patients. First pass Tc-99m sestamibi imaging of ejection fraction agreed well with conventional first-pass imaging for the right and left ventricle. It is concluded that Tc-99m sestamibi myocardial imaging at rest reliably diagnoses and localizes infarction and assesses ejection fraction by first-pass imaging.

Redistribution thallium-201 imaging 2 to 4 h after exercise may be incomplete and therefore may be inadequate to fully assess myocardial variability. Late redistribution imaging 24 h after exercise has been proposed to overcome this limitation of thallium stress imaging. However, because of poor count density the image quality on these studies is often suboptimal. In the present study the diagnostic information on 24-h planar thallium redistribution images was compared with that on images obtained after a reinjection of thallium at rest.Eighty-four patients with a stress thallium-201 defect had delayed redistribution imaging after 2 to 4 h and 24 h later, and again after an injection of thallium at rest. Defect reversibility on 24-h redistribution images was compared quantitatively with that on images after injection of thallium at rest. The quality of thallium images at rest was consistently better than that of 24-h redistribution images. Poor quality studies occurred in 13% of 24-h redistribution images compared with 0.4% of the studies at rest. Significantly more defect reversibility was detected on images after the reinjection at rest.Of 41 patients who appeared to have a fixed defect at 2- to 4-h redistribution imaging, 11 (27%) had a reversible defect by 24-h redistribution imaging compared with 29 (71%) after thallium-201 reinjection. No clinical variables at the time of stress testing were predictive of late defect reversibility. It is concluded that in patients with fixed a thallium defect at 2 to 4 h after exercise, reimaging after a reinjection at rest provides better diagnostic information than does 24-h late redistribution imaging.

Silent myocardial ischemia has been inferred from transient ST-segment depression during continuous electrocardiographic monitoring. Recently, continuous ambulatory monitoring of left ventricular (LV) function using a radionuclide technique (VEST) has demonstrated episodes of significant silent LV dysfunction in the absence of electrocardiographic changes. To validate the demonstration of silent LV dysfunction with this technique, 12 men were studied during percutaneous transluminal coronary angioplasty. A total of 18 left anterior descending coronary artery balloon inflations were performed. Balloon inflations at 8 +/- 2 atm (4 to 10 atm) lasted 70 +/- 16 seconds. Seventeen of 18 inflations were associated with a decrease in LV ejection fraction greater than 0.10. Mean LV ejection fraction decreased from 0.53 +/- 0.08 to 0.28 +/- 0.11 (p less than 0.0001). In contrast, there was pain in only 10 inflations and ST-segment changes in 7. LV dysfunction was associated with a minimal increase in end-diastolic volume (4 +/- 3%, p less than 0.003), and a major increase in relative end-systolic volume (69 +/- 43%, p less than 0.001). These data suggest that continuous monitoring of LV function with the VEST can sensitively detect silent ischemic decreases in LV function occurring during angioplasty, and provide further validation of the use of this technique for detecting silent myocardial ischemia.

Normal left ventricular systolic performance with impaired left ventricular diastolic filling may be present in a substantial number of patients with congestive heart failure (CHF). To evaluate the effect of oral verapamil in this subset, 20 men (mean age 68 +/- 5 years) with CHF, intact left ventricular function (ejection fraction greater than 45%) and abnormal diastolic filling (peak filling rate less than 2.5 end-diastolic volumes per second [edv/s]) were studied in a placebo-controlled, double-blind 5-week crossover trial. All patients underwent echocardiography to rule out significant valvular disease, and thallium-201 stress scintigraphy to exclude major active ischemia. Compared to baseline values, verapamil significantly improved exercise capacity by 33% (13.9 +/- 4.3 vs 10.7 +/- 3.4 minutes at baseline) and peak filling rate by 30% (2.29 +/- 0.54 vs 1.85 +/- 0.45 edv/s at baseline) (all p less than 0.05). Placebo values were 12.3 +/- 4.0 minutes and 2.16 +/- 0.48 edv/s, respectively (difference not significant for both). Improvement from baseline in an objective clinico-radiographic heart failure score (scale 0 to 13) was significantly greater with verapamil compared to placebo (median improvement in score: 3 vs 1, p less than 0.01). Mean ejection fraction and systolic blood pressure were unchanged from baseline; diastolic blood pressure and heart rate decreased to a small degree. Verapamil may have therapeutic efficacy in patients with CHF, preserved systolic function and impaired diastolic filling.

To investigate prospectively the occurrence and significance of postinfarction transient left ventricular dysfunction, 33 ambulatory patients who underwent thrombolytic therapy after myocardial infarction were monitored continuously for 187 +/- 56 min during normal activity with a radionuclide left ventricular function detector at the time of hospital discharge. Twelve patients demonstrated 19 episodes of transient left ventricular dysfunction (greater than 0.05 decrease in ejection fraction, lasting greater than or equal to 1 min), with no change in heart rate. Only two episodes in one patient were associated with chest pain and electrocardiographic changes. The baseline ejection fraction was 0.52 +/- 0.12 in patients with transient left ventricular dysfunction and 0.51 +/- 0.13 in patients without dysfunction (p = NS). At follow-up study (19.2 +/- 5.4 months), cardiac events (unstable angina, myocardial infarction or death) occurred in 8 of 12 patients with but in only 3 of 21 patients without transient left ventricular dysfunction (p less than 0.01). During submaximal supine bicycle exercise, only two patients demonstrated a decrease in ejection fraction greater than or equal to 0.05 at peak exercise; neither had a subsequent cardiac event. These data suggest that transient episodes of silent left ventricular dysfunction at hospital discharge in patients treated with thrombolysis after myocardial infarction are common and associated with a poor outcome. Continuous left ventricular function monitoring during normal activity may provide prognostic information not available from submaximal exercise test results.

Positron emission tomography was used to quantify changes in myocardial blood flow during mental stress in patients with and without coronary artery disease. Blunted augmentation of myocardial blood flow during mental stress was observed in regions without significant epicardial stenosis.

Forty-five patients with chronic aortic regurgitation (AR) underwent first-pass radionuclide angiocardiography (RNA) at rest and during upright bicycle exercise, as well as M-mode echocardiography at rest. Abnormal left ventricular (LV) exercise reserve, defined by the absolute change in ejection fraction (EF), was present in 16 of 45 patients (36%). Seven of ten patients with abnormal resting EF (less than 50%) and three of seven symptomatic patients had normal LV exercise responses. Patients with normal LV exercise reserve by RNA had LV dimensions by echo at end diastole (5.9 +/- 0.2 vs 6.5 +/- 0.3 cm, p = NS) and end systole (3.9 +/- 0.2 vs 4.4 +/- 0.3 cm, p = NS) comparable to those in patients wht abnormal LV exercise reserve. However, the mean corrected LV end-diastolic (LVED) radius/wall thickness ratio was significantly greater in AR patients with abnormal LV exercise reserve than in those with normal LV exercise reserve (395 +/- 15 vs 315 +/- 16, p less than 0.01). There data suggest that resting echocardiographic LV dimensions as well as the corrected echo LVED radius/wall thickness ratio have a variable relationship to RNA LV exercise performance in patients with chronic AR.

Because right ventricular ejection fraction (RVEF) depends on impedance to RV ejection, the hypothesis was tested that an abnormality in radionuclide-determined RVEF would be a useful noninvasive predictor of pulmonary artery (PA) hypertension in patients with chronic obstructive pulmonary disease (COPD). Simultaneous measurements of resting RVEF and PA pressure were made in 30 patients with COPD. All were stable and without clinical evidence of respiratory decompensation or congestive heart failure. Eleven patients had normal (less than 20 mm Hg) mean PA pressure and 19 patients had PA hypertension. The average RVEF was 41 +/- 7% (range 29 to 60%). Five patients had normal (greater than 45%) and 25 patients depressed RVEF. An inverse linear relation between mean PA pressure and RVEF was present (r = -0.74). In the group with normal PA pressure, RVEF averaged 48% (range 42 to 60%). In the group with PA hypertension, RVEF averaged 36% (range 29 to 44%). RVEF was significantly higher in the group with PA hypertension. Using RVEF less than 45% as an indicator of PA hypertension, the sensitivity was 100%, the specificity 55%, and the predictive accuracy of a positive result 79%. Using RVEF less than or equal to 40% as an indicator of PA hypertension, the sensitivity was 75%, the specificity 100%, and the predictive accuracy of a positive study 100%. Thus, radionuclide-determined RVEF using the first-pass technique and a multicrystal camera is a useful noninvasive test for diagnosing PA hypertension in patients with advanced COPD.

In Thrombolysis in Myocardial Infarction (TIMI) Phase I,290 patients with acute myocardial infarction were randomized to either intravenous recombinant tissue-type plasminogen activator (rt-PA) or intravenous streptokinase. Two hundred twenty-nine patients had radionuclide ventriculograms at discharge for assessment of global and regional left ventricular ejection fraction. Among these 229 patients 185 had totally occluded infarct-related arteries, and angiographic reperfusion of the infarct-related artery occurred in 69% of patients treated with rt-PA and 28% of patients treated with streptokinase (p less than 0.001). Mean global left ventricular ejection fraction was not different for rt-PA-treated patients compared with streptokinase-treated patients (0.46 versus 0.45). However, the average regional ejection fraction of the regions subtended by the infarct-related artery showed a trend toward better average infarct region ejection fraction in patients treated with rt-PA than in patients treated with streptokinase (0.40 versus 0.36; 0.05 less than p less than 0.06). Analysis of data according to perfusion status of the infarct-related artery showed no difference in mean global left ventricular ejection fraction between patients with sustained versus nonsustained reperfusion (0.47 versus 0.44). However, there was better average regional ejection fraction of the region subtended by the infarct-related artery in patients with sustained reperfusion (0.40 versus 0.36; p less than 0.01). Thus, quantitation of regional left ventricular function by radionuclide techniques provides a noninvasive means for evaluating the effects of thrombolysis. This study suggests a direct relation between improvement of regional left ventricular function and the greater infarct-related artery patency rate achieved by rt-PA compared with streptokinase.

To study the influence of ischemia on both early and late left ventricular filling, Doppler 2-dimensional echocardiography was used to measure filling parameters during percutaneous transluminal coronary angioplasty (PTCA) in 26 patients. Doppler recordings were taken immediately before balloon inflation and continuously during balloon inflation and deflation until 60 seconds into the recovery period. During PTCA of the left anterior descending artery (16 patients) there was a 35% decrease in early peak filling rate from 269 +/- 88 to 169 +/- 55 ml/s (p less than 0.0005) by 60 seconds of balloon inflation. In patients undergoing PTCA of the left circumflex (4 patients) or dominant right coronary artery (6 patients), the early peak filling rate decreased 15% from 325 +/- 126 to 284 +/- 137 ml/s (p less than 0.005). The decrease in early peak filling rate became evident at approximately 15 seconds after balloon inflation and fully recovered 20 seconds after balloon deflation. Rather than an expected increase in atrial stroke volume and a decrease in early to late filling ratio during coronary occlusion, there was a 28% decrease in atrial stroke volume during left anterior descending coronary artery PTCA and a 6% decrease during right coronary and circumflex PTCA. Because of the simultaneous decrease in both early and late ventricular filling, peak early to late filling ratio was only slightly altered during PTCA. There was an 83% increase in mean pulmonary artery wedge pressure during balloon inflation from 12 +/- 5 to 20 +/- 4 mm Hg. In 11 of these patients global systolic function was measured on subsequent inflations during PTCA using 2-dimensional echocardiography.(ABSTRACT TRUNCATED AT 250 WORDS)

The pathophysiologic correlates of right ventricular ejection fraction, as well as its relation to contractile function as assessed by systolic pressure-volume data, were evaluated in 20 patients with chronic obstructive pulmonary disease. Radionuclide and hemodynamic measurements were obtained simultaneously. Baseline determinations were obtained in all patients. In seven patients, studies were repeated after intravenous administration of sodium nitroprusside. This procedure allowed characterization of right ventricular performance at decreased afterload and provided two points necessary for definition of the right ventricular systolic pressure-volume relation. Seventeen of the 20 patients had a depressed right ventricular ejection fraction (less than 45 percent). There was a strong inverse linear correlation between right ventricular ejection fraction and afterload as assessed by peak or mean pulmonary arterial pressure (r = −0.81) and pulmonary vascular resistance index (r = −0.73). Right ventricular ejection fraction also correlated, although less strongly, with preload as assessed by right ventricular end-diastolic volume index (r = −0.56) and mean right atrial pressure (r = −0.51). It did not correlate with cardiac index, the ratio of peak pulmonary arterial pressure to right ventricular end-systolic volume index, arterial oxygen tension or left ventricular ejection fraction. After nitroprusside administration, mean arterial pressure, peak pulmonary arterial systolic pressure and pulmonary vascular resistance index decreased significantly. The slope (E) and the volume intercept (V 0 ) of each pressure-volume line were determined. Administration of dobutamine resulted in a leftward shift from the endsystolic pressure-volume line. There were poor correlations between E and right ventricular ejection fraction, as well as between E and the control ratio between pulmonary arterial systolic pressure and end-systolic volume index. These data demonstrate that, in addition to intrinsic contractile influences, right ventricular ejection fraction is highly dependent on afterload, but less dependent on preload. Right ventricular ejection fraction is a poor indicator of the slope of the systolic pressure-volume relation, raising questions concerning its use as an independent index of chamber contractility.

Twenty-three surviving patients who were weaned from cardiopulmonary bypass with intraaortic balloon pump assistance returned for follow-up radionuclide left ventricular (LV) function and thallium 201 perfusion studies at a mean of 23 +/- 3 months following operation. It was found tat despite profound intraoperative myocardial depression requiring intraaortic balloon assistance, 13 patients had no change (within 10%) in the resting LV ejection fraction compared with the preoperative measurement. Among all 23 patients, there was no difference between mean (+/- standard error of the mean) preoperative and postoperative resting LV ejection fraction (48 +/- 4 vs 46 +/- 4%, p = not significant [NS]). Only 11 patients had perioperative myocardial infarction documented by new Q waves in the electrocardiogram, by elevation of creatine kinase-MB fraction, or by defects on thallium 201 imaging not explained by documented myocardial infarction before operation. Overall, postoperative resting LV ejection fraction was not different from the preoperative value in patients with perioperative myocardial infarction (44 +/- 7 vs 47 +/- 5%, p = NS). Postoperative resting LV ejection fraction rose by greater than 10% compared with preoperative values in 4 patients (3 with aortic valve replacement), remained within the 10% limit in 9 patients, and fell by greater than 10% in 10 patients (7 with perioperative myocardial infarction). Only 4 out of 16 patients studied at follow-up with exercise radionuclide studies demonstrated a normal LV response to exercise (greater than 5% increase in LV ejection fraction). Thus, among survivors requiring intraaortic balloon pump assistance for weaning from cardiopulmonary bypass, LV performance at rest is frequently preserved. In addition, 11 of the 23 patients had evidence of perioperative myocardial infarction, indicating a component of reversible intraoperative LV dysfunction.

Using serial invasive hemodynamics in concert with noninvasive radionuclide monitoring of left ventricular (LV) function, 20 patients with unstable angina were evaluated during incremental infusion of intravenous nitroglycerin. Of 20 patients, 17 demonstrated a favorable hemodynamic response and dose responses could be determined for individual patients. There was excellent agreement between hemodynamic and noninvasive radionuclide measurements, and patient responses could be inferred from the radionuclide data alone. Cardiac output improved by 29% (mean 4.7 +/- 1.2 to 6.0 +/- 1.3), LV ejection fraction increased an average of 0.11 (0.39 +/- 0.14 to 0.50 +/- 0.16) and diastolic function as assessed by peak filling rate improved from 1.80 +/- 0.60 end-diastolic volumes/s to 2.70 +/- 0.90. Changes in systolic blood pressure and heart rate were not predictive of hemodynamic response. The dose of nitroglycerin necessary to produce maximal hemodynamic benefit was variable (mean 98 micrograms/min, range 48 to 144). In 7 patients, nitroglycerin caused excessive decreases in pulmonary arterial wedge pressure and adverse hemodynamics that corrected with intravenous fluids, allowing continued administration of intravenous nitroglycerin with improvement in hemodynamic status. In 15 patients, peak systolic pressure--end-systolic volume relations were assessed to define possible changes in LV contractility induced during nitroglycerin infusion. In 12 of these patients, this relation was linear, suggesting altered loading rather than augmented contractility as nitroglycerin's mechanism of action. In 3 patients a downward and rightward shift of the systolic relation was seen, suggesting that significant underloading with nitroglycerin was associated with depressed contractility.

To impact on the development of clinical congestive heart failure as a complication of doxorubicin therapy, left ventricular ejection fraction was monitored with serial resting radionuclide angiocardiography in 1,487 patients with cancer over a seven-year period in both university and community hospital environments. A high-risk subset of 282 patients was selected for retrospective analysis of their clinical outcome. High-risk patients were identified by one or two of the following three criteria: decline of 10 percent or more in absolute left ventricular ejection fraction from a normal baseline to 50 percent or less; high cumulative dose of doxorubicin (more than 450 mg/m2); abnormal baseline left ventricular ejection fraction (less than 50 percent). Clinical congestive heart failure occurred in 46 (16 percent) during the treatment period, and in an additional three patients (1.3 percent) at last follow-up examination 11.8 +/- 14.2 months following discontinuation of doxorubicin. Total cumulative dosages of doxorubicin that precipitated congestive heart failure (75 to 1,095 mg/m2) and those that did not (30 to 880 mg/m2) varied widely. Decline of 10 percent or more in absolute left ventricular ejection fraction to a value of 50 percent or less preceded administration of the final dose of doxorubicin that precipitated clinical congestive heart failure in the majority of patients in whom congestive heart failure developed. Clinical congestive heart failure improved in 87 percent given routine therapy with digitalis, diuretics, and/or vasodilators. Criteria for monitoring left ventricular ejection fraction and discontinuing doxorubicin were formulated. The occurrence of clinical congestive heart failure was compared in those patients whose management was concordant with proposed criteria (Group A) and in those whose management was not (Group B). Group A had a lower incidence of congestive heart failure compared with Group B (2.9 percent versus 20.8 percent, p less than 0.001) and had only mild congestive heart failure that resolved with treatment (n = 2) and no deaths due to congestive heart failure. Multivariate analysis with proportional-hazards regression (Cox's model) demonstrated a fourfold reduction in the incidence of congestive heart failure independent of other clinical predictor variables in those patients whose management was concordant with proposed guideline criteria. The incidence, persistence, late development, predictability, and reversibility of clinical congestive heart failure were comparable in university and community hospital settings.(ABSTRACT TRUNCATED AT 400 WORDS)

In summary, nuclear techniques have important roles in both the acute and convalescent phase of MI. Acutely, both myocardial perfusion and ventricular function may be assessed. In patients treated with thrombolytic therapy, perfusion imaging, and metabolic imaging using PET may be able to delineate ischemic myocardium. These techniques are being developed to accurately quantify salvaged myocardium for assessing the efficacy of an acute intervention, and to characterize (functionally) the remaining myocardium for possible further intervention. In the convalescent phase, prognostic information is obtained from both rest and exercise evaluation of ventricular function and reserve, ambulatory monitoring, as well as from the presence of exercise-induced ischemia as documented by quantitative thallium imaging. The results of these studies can be used to determine appropriate management strategies.

The acute hemodynamic and functional effects of the relatively selective beta2 adrenoreceptor agonist, terbutaline, was evaluated in a well defined group of eight patients with chronic obstructive pulmonary disease, abnormal right ventricular performance and elevated pulmonary vascular resistance. Radionuclide and hemodynamic data were obtained simultaneously using first pass radionuclide angiocardiography and thermodilution pulmonary arterial catheterization. Terbutaline caused no change in right ventricular end-diastolic volume index but increased right ventricular stroke work index from 13 ±5 to 16 ± 6 g · m/m2 (mean ± standard deviation; p < 0.025). Furthermore, pulmonary vascular resistance index decreased in all patients and for the group decreased from 623 ± 279 to 407 ± 204 dynes · s · cm−5 · m2 (p < 0.05). The extent of this decrease correlated linearly with the level of resting pulmonary vascular resistance (r = 0.76). Right ventricular ejection fraction increased significantly from 35 ± 10 to 46 ± 5 percent; terbutaline resulted in normalization (to greater than 45 percent) of the ejection fraction in five of the eight patients. The changes in right ventricular ejection fraction were greatest in patients with the highest level of pulmonary vascular resistance and the lowest baseline ejection fraction. Left ventricular ejection fraction also increased significantly from 62 ± 10 to 71 ± 10 percent; however, there was no correlation between the change in this variable and either systemic vascular resistance or baseline left ventricular ejection fraction. Systemic oxygen delivery increased from 45 ± 16 to 63 ± 19 ml/min per m2 (p < 0.005) without any change in arterial oxygen tension. This study demonstrates that terbutaline results in substantial augmentation of right ventricular performance. This effect appears to be mediated predominantly through alterations in pulmonary vascular resistance. Terbutaline may provide significant cardiac benefits in addition to its salutory effects on the tracheobronchial tree.

Although oral theophylline is a widely used bronchodilator in chronic obstructive pulmonary disease (COPD), its effects upon cardiac performance have not been fully established. The effect of slow release oral theophylline upon right ventricular and left ventricular ejection fraction was evaluated using first-pass quantitative radionuclide angiocardiography in 15 patients with COPD. After 72 hours of therapy, oral theophylline significantly increased right ventricular ejection fraction (42% to 48%, p less than 0.005). In 7 of 10 patients with depressed baseline right ventricular performance, including two with cor pulmonale, right ventricular ejection fraction normalized (greater than or equal to 45%). After long-term therapy, an average of 16 weeks, right ventricular fraction also increased (43% to 48%, p less than 0.005). Left ventricular ejection fraction improved significantly from 64% to 68% (p less than 0.05) at 72 hours and from 61% to 65% (p less than 0.025) after long-term therapy. These data indicate that oral theophylline produces a sustained modest enhancement of resting biventricular performance in COPD.

The efficacy of 1-vessel percutaneous transluminal coronary angioplasty (PTCA) directed at the presumed angina-producing stenosis, or "culprit lesion," in the treatment of unstable angina pectoris and multivessel coronary artery disease (CAD) was assessed in 27 patients with unstable angina refractory to optimal medical therapy. Eighteen patients had 2-vessel and 9 had 3-vessel CAD. The culprit lesion was identified in all patients by analysis of the qualitative appearance of the coronary lesions and detection of angiographic evidence of plaque fissuring or coronary thrombosis. Intracoronary filling defects were evident in 26% and eccentric stenoses with irregular edges were noted in 41% of patients. Subtotal obstructions were seen in 33%. Confirmation of the identity of the culprit lesion was also available in 78% of patients by analysis of the pattern and distribution of spontaneous electrocardiographic changes. The PTCA primary success rate was 89%, with no procedure-related complications. All patients in whom PTCA was successful had immediate resolution of their unstable angina. Follow-up of the successfully treated patients after a mean of 16 months (range 12 to 20) showed maintenance of long-term clinical improvement, with only 17% of patients having recurrent angina. These data suggest that 1-vessel PTCA of the culprit lesion may serve as a feasible therapeutic option in the treatment of selected patients with multivessel CAD and unstable angina.

The association of a left coronary artery-main pulmonary artery fistula and an anomalous right coronary artery originating from the main pulmonary artery is the subject of this report. This unique combination of congenital cardiac anomalies establishes a double coronary steal from the left coronary artery, which hemodynamically represents the sole source of myocardial perfusion. The left coronary artery-main pulmonary artery fistula was closed and the coexisting anomalous right coronary artery reimplanted into the anterior aspect of the ascending aorta. A dual coronary supply was therefore established and thus eliminated the potential threat of total myocardial ischemia should the left coronary artery become critically compromised. Patency of both the left coronary artery and the transplanted right coronary artery was documented 1 year postoperatively by aortic root angiography.

To assess the efficacy of intravenous streptokinase in patients with acute myocardial infarction, 40 patients (30 men and 10 women, mean age 54 years) with acute myocardial infarction were given 1.5 million U of streptokinase intravenously in 1 hour, and coronary arteriography was performed repeatedly to assess reperfusion. Streptokinase treatment was begun 270 +/- 86 (mean +/- SD) minutes after the onset of chest pain. Of the 40 patients, 34 had total or near total coronary occlusion before streptokinase administration. In 14 (41%) of these 34 patients, some reperfusion occurred during the 90 minutes after the administration of streptokinase, but in only 11 of the 14 was reperfusion present at 90 minutes. After streptokinase administration, all patients received heparin for 8 to 10 days; they were subsequently administered aspirin and dipyridamole. Clinical evidence of reocclusion during the first 24 hours of heparin therapy occurred in one patient. Thus, when given to patients with acute myocardial infarction and total coronary occlusion an average of 4 1/2 hours after the onset of chest pain, high dose intravenous streptokinase achieves reperfusion in only about 40% and results in sustained reperfusion in only about 30%.

Left ventricular performance was monitored serially in 25 patients during laryngoscopy and intubation in the anesthetic induction period before elective coronary artery bypass surgery using the labeled equilibrium blood pool and the computerized nuclear probe. Left ventricular ejection fraction was obtained preoperatively, after induction of anesthesia but before endotracheal intubation, immediately after intubation, and at 1 minute intervals thereafter for 10 minutes. In all patients, there was an immediate decrease (mean 16%) in left ventricular ejection fraction accompanying the reflex hypertension and tachycardia occurring during laryngoscopy and endotracheal intubation; it was significantly depressed for 3 minutes with the concomitant hemodynamic changes. Seven patients did not demonstrate a recovery of left ventricular ejection fraction to the preintubation value. In 10 healthy noncardiac patients undergoing orthopedic surgery, after an identical anesthetic induction sequence and intubation, there was a similar decrease in ejection fraction, but of shorter duration. In these patients the recovery of left ventricular performance preceded the recovery of blood pressure and heart rate. This study demonstrates that profound decreases in left ventricular performance accompany the reflex hypertension and tachycardia occurring during endotracheal intubation and that there is persisting depression of left ventricular function in some patients with coronary artery disease. These findings indicate the potential utility of the computerized nuclear probe for monitoring ventricular performance during this critical period.

The emergence in the past 20 years of nuclear medicine as a distinct diagnostic discipline has been a major clinical advance. The relatively rapid evolution from the small laboratory limited primarily to the study of thyroid disease to the large unit in which radioactive tracers (radionuclides) are utilized to evaluate structure and function of most organ systems has been accelerated by major advances in instrumentation, new radioactive tracers and application of computer techniques. Application of these radionuclide techniques to the study of coronary artery disease has been quite recent, and has in part been limited by the need for a coordinated effort between the cardiologist and the specialist in nuclear medicine. However, realization of the potential usefulness of these techniques has fostered an increasingly productive liaison between the two specialties. The potential advantages of these radionuclides in evaluating patients with cardiovascular disease is twofold: first, they may permit the noninvasive or atraumatic acquisition of data that might otherwise be obtained only at the time of cardiac catheterization; second, and perhaps more important, they may permit the acquisition of physiologic measurements or observations not attainable by more conventional modes of study. Functionally, these techniques can be divided into those that evaluate cardiac performance and those that evaluate coronary blood flow, regional myocardial perfusion and myocardial viability.

Although aminophylline is a widely used bronchodilator in chronic obstructive pulmonary disease (COPD), its effects upon cardiac performance have not been fully established. The effect of aminophylline upon right ventricular and left ventricular ejection fraction and the left ventricular ejection rate was evaluated by first-pass quantitative radionuclide angiocardiography in 15 patients with COPD, including four with cor pulmonale, and in five control subjects without cardiopulmonary disease. Aminophylline infusion (9 mg/kg) significantly increased the right ventricular ejection fraction (45 to 52 per cent), left ventricular ejection fraction (60 to 67 per cent) and left ventricular ejection rate (3.4 to 4.1 sec −1 ) in patients with COPD (all parameters, p −1 ) (p 1 ) and forced vital capacity (FVC) increased significantly in patients with COPD but not in control subjects. Arterial carbon dioxide tension decreased significantly in both groups (p These data indicate that aminophylline acutely enhances biventricular performance in COPD. Since comparable cardiovascular changes are induced in normal subjects in whom ventilatory function was not altered, the beneficial effects of aminophylline upon global ventricular performance appear to be independent of the degree of pulmonary compromise.

Thirty-eight men who suffered acute transmural myocardial infarction before age 40, and after recovery were New York Heart Association functional Class I or II, were studied by noninvasive means and by coronary angiography in order to determine whether these nonivasive studies could predict the presence of significant coronary artery disease remote from that felt to be responsible for the previous myocardial infarction. Patients were divided into two groups on the basis of the absence (Group I) or presence (Group II) of obstructive disease in a major coronary artery supplying myocardium remote from the prior myocardial infarction. There were 21 patients in Group I and 17 patients in Group II. They did not differ with respect to age, abnormalities of lipid or glucose metabolism, family history, history of hypertension or cigarette use, presence of obesity, or infarct localization. Ten of 17 patients in Group II had angina pectoris; only 3/21 patients in Group I had angina pectoris (p less than 0.01). All 12 patients tested in Group II had a positive maximal exercise tolerance test; only 1/17 patients tested in Group I was similarly positive (p less than 0.001). The absence of angina pectoris and the presence of a negative maximal exercise tolerance test is strong evidence against the pressure of significant CAD remote from that responsible for the prior myocardial infarction.

Left ventricular hypertrophy is associated with decreased longevity and often leads to congestive heart failure. An exploratory study of magnetic resonance imaging in human left ventricular hypertrophy was performed. First, 13 patients with left ventricular hypertrophy and 7 controls of similar ages were studied using electrocardiogramgated end-diastolic images. Visual inspection suggested that low-intensity zones were frequently found within the hypertrophied myocardium. To verify this observation, the images were processed with semi-automatic edge detection and a derivative-based tissue characterization algorithm, yielding tissue heterogeneity indices (THI-A and THI-V) which objectively measured the low-intensity zones. THI-A and THI-V were both significantly greater in left ventricular hypertrophy patients than in controls (THI-A: 0.111 vs 0.038, p = 0.009). THI was also significantly correlated with duration of disease and electrocardiographic abnormalities. To validate these initial findings prospectively, the same quantitative analysis was applied to magnetic resonance images of an additional 20 left ventricular hypertrophy patients and 12 controls from two institutions, using different imaging systems and different acquisition parameters. Again, THI was significantly greater in patients than in controls. Analysis of end-systolic images yielded similar results. In four dogs with left ventricular hypertrophy induced by aortic banding, THI showed a statistically significant increase as left ventricular hypertrophy developed. Hypertrophied myocardium thus shows reproducible differences from normal tissue with magnetic resonance imaging; hence, quantitative magnetic resonance tissue characterization may be useful in assessing pathologic changes in LVH.

Thirty-six patients with diverse baseline right ventricular function were evaluated during incremental positive end-expiratory pressure (PEEP) application. Right heart pressures, cardiac output, right ventricular ejection fractions, and ventricular volumes were obtained at each PEEP level. Right ventricular peak systolic pressure-end-systolic volume relations were analyzed as an index of contractile function. Patients with severely depressed baseline right ventricular ejection fractions (30 percent or less) had an increase in end-diastolic (270 ± 74 to 391 ± 76 ml, 0 to 20 cm water (H 2 O) PEEP, p 2 O PEEP, p 2 O PEEP as estimated by the slope of systolic pressure-volume relations (0.12 to 0.04 mm Hg/ml, 0 to 15 and 15 to 20 cm H 2 O PEEP, respectively, p

The relation of degree of regional wall motion abnormality by equilibrium radionuclide angiocardiography to the presence and mural extent of regional necrosis or scar at autopsy was evaluated in 23 autopsy patients who had a history of myocardial infarction and had equilibrium radionuclide angiocardiography within 40 days of death. Of the 228 regions evaluated by equilibrium radionuclide angiocardiography, 135 had abnormal regional wall motion and 102 (76%) of these 135 regions had evidence of myocardial infarction at autopsy. The overall sensitivity, specificity and predictive values of regional wall motion abnormality for regional necrosis or scar were 69, 59 and 76%, respectively. Of the 33 false positive regions, 20 (61%) had severe narrowing of the coronary artery supplying that region, 13 (39%) were adjacent to a region with a myocardial infarction and almost half (16 [48%]) were in the lateral wall. Eighty-three (36%) of the 228 regions were akinetic or dyskinetic, 52 (23%) were hypokinetic and 93 (41%) were normal. Sixty-three (76%) of the 83 akinetic/dyskinetic segments had transmural myocardial infarction at autopsy, 14 (17%) had nontransmural myocardial infarction and only 6 (7%) contained no necrosis or scar. In contrast, 14 (27% ) of 52 hypokinetic segments had transmural myocardial infarction, 11 (21%) had nontransmural myocardial infarction and 27 (52%) were normal. Thus, the most severe regional wall motion abnormality (akinesia/dyskinesia) almost always indicates regional myocardial infarction which is usually transmural whereas less severe dysfunction (hypokinesia) is not necessarily associated with regional necrosis or scar. The severity of regional dysfunction must be considered if equilibrium radionuclide angiocardiography is used to evaluate the presence and mural extent of myocardial infarction within a region.

First pass radionuclide angiocardiography and thallium-201 myocardial perfusion imaging were performed at rest and during exercise in 48 patients with chest pain: 39 with angiographically documented coronary artery disease and 9 with normal coronary arteries. Maximal graded upright bicycle exercise was used for both studies to assure identical exercise conditions. All nine patients without coronary artery disease had normal exercise thallium images, normal exercise regional wall motion and at least a 5 percent absolute increase in left ventricular ejection fraction during exercise (normal exercise left ventricular reserve). Ischemic S-T segment depression was demonstrated in 17 (44 percent) of the 39 patients with coronary artery disease. Findings on the two exercise tests were concordant in all cases. New or augmented thallium perfusion defects were detected in 24 (62 percent) of the 39 patients, whereas abnormal exercise left ventricular reserve was present in 33 (85 percent) (p