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Several studies have demonstrated a correlation between myocardial ischemia and severity of coronary lesions as determined by intravascular ultrasound (IVUS) and fractional flow reserve (FFR) measurements. However, their value for the assessment of mild coronary stenoses that are associated with myocardial perfusion abnormalities has not been well studied. The objective of this study was to prospectively compare the results of myocardial perfusion as determined by exercise/dipyridamole myocardial single-photon emission computed tomography with IVUS and FFR measurements in patients who had angiographically mild coronary stenosis (50% diameter stenosis by quantitative coronary angiography). Forty-eight patients who had stable coronary disease (61 +/- 11 years of age; 6 women) were included. All had mild coronary stenosis in the proximal/middle segment ofor = 1 coronary artery and had undergone maximal exercise myocardial technetium-99m tetrofosmin single-photon emission computed tomography within 48 hours before coronary angiography. IVUS measurements included lesion lumen area, external elastic membrane area, lesion plaque burden (calculated as external elastic membrane minus lumen area, divided by external elastic membrane, and multiplied by 100), and lumen area stenosis (calculated as reference lumen area minus lesion lumen area, divided by reference lumen area, multiplied by 100). Fifty-three coronary lesions were studied, with a mean percent diameter stenosis of 34.9 +/- 7.9% on angiography. Myocardial perfusion defects were demonstrated by single-photon emission computed tomography in 11 patients (12 myocardial regions) with no differences in lesion percent diameter stenosis compared with those without perfusion defects. The presence of reversible perfusion defects was associated with a higher lesion plaque burden as evaluated by IVUS (67.4 +/- 8.1% vs 60.2 +/- 9.3%, p = 0.01). FFR values did not differ in the presence or absence of perfusion defects (0.90 +/- 0.06 vs 0.92 +/- 0.07, respectively; p = NS). In conclusion, plaque burden as determined by IVUS may partly explain the presence of myocardial perfusion defects in cases of angiographically nonsignificant coronary lesions. However, the high FFR values associated with these lesions suggest that other mechanisms, such as endothelial/microvascular dysfunction, might also account for perfusion abnormalities in these patients.

To demonstrate that the administration of dipyridamole at the end of an insufficient maximal subjective exercise test can improve the diagnostic accuracy of single-photon emission computed tomography in patients with previous myocardial infarction, 209 consecutive patients were studied with technetium-99m methoxyisobutyl isonitrile single-photon emission computed tomography and coronary angiography. Patients were divided in 3 groups: group 1, 107 patients with sufficient exercise testing; group 2, 55 patients with insufficient exercise testing; group 3, 47 patients with insufficient exercise testing in whom intravenous dipyridamole (0.56 mg/kg over 4 minutes) was administered at the end of exercise. In groups 1 and 3 the sensitivity values for the diagnosis of multivessel disease were significantly higher (80% and 76%, respectively) than those in group 2 (59% [p = 0.009 and p = 0.02, respectively]). Specificity and predictive values were not different among the 3 groups. Thus, in patients with previous infarction in whom adequate levels of exercise could not be achieved, dipyridamole administration at the end of exercise significantly increased the sensitivity for diagnosing multivessel disease.

The aim of this study was to assess the prognosis of medically treated patients with “clandestine” myocardial ischemia (perfusion defect without angina and no ST depression >1 mm during exercise test) compared to those with silent myocardial ischemia (ST-segment depression >1 mm, without angina) and those with angina pectoris. One hundred twelve patients without previous myocardial infarction were included. All patients underwent a symptom-limited exercise test on a bicycle ergometer, myocardial perfusion technetium-99m-methoxy-isobutyl-isonitrile single-photon emission computed tomography (SPECT), and coronary angiography. They were classified into 3 groups (angina group, 34 patients; silent group, 20 patients; and the clandestine group, 58 patients). The mean follow-up was 3.6 years (range 6 months to 5.5 years). Patients with clandestine ischemia had a lower scintigraphic and angiographic score than patients with silent ischemia (25 ± 8 vs 31 ± 9 and 24 ± 8 vs 29 ± 7, p = 0.008, respectively), but the prognosis was similar. Only angina and severe reversible SPECT defects were predictive for cardiac events: death + myocardial infarction + revascularization. We conclude that in medically treated patients without previous myocardial infarction, angina and severe reversible SPECT defects are predictive for cardiac events only when the need for revascularization is included as a cardiac event.

Patients with ventricular septal (VS) rupture (n = 96) or left ventricular (LV) free wall rupture (n = 97) during acute myocardial infarction had comparable clinical, angiographic, and electrocardiographic features, suggesting similar underlying mechanisms, although the 2 groups differed in the rate of bundle branch block, complete atrioventricular block, atrial fibrillation, and culprit artery. In 20 patients, LV rupture followed VS rupture, which underscores the need for early surgery.

Seventeen of 31 patients with papillary muscle rupture (PMR) were admitted with a >24-hour delay since onset of acute myocardial infarction (AMI) in contrast to 81 of 1,012 with AMI without cardiac rupture; in 8 of 11 patients with in-hospital PMR it was preceded by new anginal pain in 5 and/or by strenuous exercise in 4; mortality was higher in those with anterior PMR, previous infarction, or 3-vessel disease than in those without PMR. Thus, persistence of physical activity before or during hospitalization, as well as postinfarction ischemia/infarct extension, appear to be relevant triggers of PMR, whereas mortality is more often associated with existence of a previous infarction, 3-vessel disease, and/or anterior PMR.

Patients with variant angina pectoris showed greater serotonin plasma levels than did control subjects and patients with healed myocardial infarction. The levels also tended to be greater in those with >1 episode/month than in those with fewer episodes. Moreover, patients with variant angina pectoris also had greater levels of nitrite and nitrate plasma levels than did control subjects or patients with healed myocardial infarction, partly, perhaps, as a compensatory mechanism.

Thus, painful LBBB has a good prognosis concerning long-term myocardial infarction or mortality. Progression to a permanent LBBB with disappearance of chest pain is frequent. Clinical surveillance is recommended because complete atrioventricular block and depression of left ventricular systolic function can be observed in rare cases.

To assess the extent of myocardial necrosis and ischemia in patients with anterior wall healed myocardial infarction depending on whether ST-segment elevation was present on precordial leads during exercise testing, 62 consecutive patients (49 men and 13 women, age [mean +/- SD] 56 +/- 11 years) with anterior wall infarcts were assessed with exercise technetium-99m (Tc-99m) methoxy-isobutyl-isonitrile single-photon emission computed tomography and quantification of the extent of necrosis and ischemia on polar maps: 22 patients hador = 1 mm ST-segment elevation during exercise, and 40 did not. The extent of the necrosis in the anteroseptal (p = 0.001) and apical (p = 0.002) regions, the extent of ischemia in the lateral region (p = 0.003) on polar maps, and the frequency of ventricular aneurysm as shown by cardiac catheterization (p = 0.001) were significantly greater in patients with ST-segment elevation. In a multiple logistic regression model, both extent of necrosis in the anteroseptal region (odds ratio 10.8; 95% confidence interval 2.7 to 44.0) and extent of ischemia in the lateral region (odds ratio 7.25; 95% confidence interval 1.6 to 32.7) were associated with exercise-induced ST-segment elevation. These data suggest that ST-segment elevation in anterior infarctions is associated with wider necrosis in the anteroseptal and apical regions, with a wider extent of ischemia in the lateral region and a higher frequency of ventricular aneurysm. Consequently, it cannot be used as a marker of viability.

Clinical and electrocardiographic features of 227 patients who died of an acute myocardial infarction (AMI) were compared with those of 150 survivors of a first AMI. Left ventricular (LV) free wall rupture was found in 93 patients aged50 years, but not in 134. The incidence of healed infarct (4 [4%] vs 50 [37%], p0.001), heart failure (11 [12%] vs 112 [84%], p0.001), and bundle branch block (11 [12%] vs 54 [40%], p0.001) was lower in patients with than without LV rupture. In patients with anterior AMI and early rupture (1 day), admission ST elevation was higher than in those with late LV rupture (1 day, 6.8 +/- 4.0 vs 4.0 +/- 2.7 mm, p0.01). However, lateral wall AMI had minimal ST elevation and accounted for 10% of ruptures. On day 2, the decrease in ST segment in patients with late LV rupture was less than in survivors (0.5 +/- 1.6 vs 3.2 +/- 2.9 mm, p0.001). Admission systolic blood pressure in patients who had early rupture was higher than in survivors (155 +/- 22 vs 137 +/- 22 mm Hg, p0.001) and in those with late rupture (135 +/- 23 mm Hg, p0.001). Late rupture was associated with infarct thinning and triggered by a physical strain in 18 of 45 patients (40%); infarct thinning, however, was present only in 4 of 48 patients (8%) with early rupture (p0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

To assess the influence of mitral regurgitation (MR) on the response to captopril therapy for congestive heart failure (CHF), 30 patients with idiopathic dilated cardiomyopathy in New York Heart Association functional class III were studied. Left ventricular end-diastolic diameter and stroke volume were measured by Doppler echocardiography, and exercise tolerance by exercise testing before and at 1, 3 and 12 months after treatment. Patients were classified into 2 groups: those with (n = 14) and those without (n = 16) MR. No significant differences were observed between the 2 groups in pretreatment studies. Exercise tolerance increased significantly in the group with MR (p less than 0.001) during the year of follow-up, from 514 +/- 193 seconds at baseline study to 671 +/- 178 seconds (p less than 0.0005) at 1 month, 688 +/- 127 seconds (p less than 0.0005) at 3 months and 690 +/- 108 seconds (p less than 0.01) at 12 months. The group without MR had no significant changes. Stroke volume increased significantly only in the MR group during follow-up (p less than 0.01), changing from 43 +/- 9 ml at baseline study to 52 +/- 11 ml (p less than 0.01) at 1 and 49 +/- 11 ml (p less than 0.01) at 3 months. At 12 months the increase was not statistically significant. Left ventricular end-diastolic diameter decreased more in the group with than without MR, although the differences were not significant. Thus, the presence of dynamic MR appears to be an important factor in the therapeutic response to captopril therapy for CHF.

The echocardiographic (echo) features of idiopathic hemochromatosis (IH) were studied in 22 patients. Results were compared with a control group of 22 patients without heart disease. Statistically significant increases in left ventricular (LV) mass, end-diastolic and end-systolic diameters of the left ventricle and in left atrial dimension were observed in patients with IH; significant changes of systolic function indexes (decrease in fractional shortening and ejection fraction and increase in distance of the E point to the septum) were seen as well. These echo abnormalities were mainly seen in patients with abnormal electrocardiograms. In 11 patients with IH, iron removal therapy was carried out by means of periodic phlebotomies. In patients with impaired LV function at the beginning of therapy, comparison between measurements of the initial echo and posttreatment echo showed significant improvement in LV diameters, fractional shortening, ejection fraction, distance from the E point to the septum, LV mass and left atrial dimension.

A series of 231 patients with "primary" acute pericardial disease (acute pericarditis or tamponade presenting without an apparent cause) were studied according to the following protocol: general clinical and laboratory studies (stage I), pericardiocentesis (stage II), pericardial biopsy (stage III) and blind antituberculous therapy (stage IV). In 32 patients (14%) a specific etiologic diagnosis was obtained (13 with neoplasia, 9 with tuberculosis, 4 with collagen vascular disease, 2 with toxoplasmosis, 2 with purulent pericarditis and 2 with viral pericarditis). "Diagnostic" pericardiocentesis (32 patients) was performed when clinical activity and effusion persisted for longer than 1 week or when purulent pericarditis was suspected, whereas "therapeutic" pericardiocentesis (44 patients) was performed to treat tamponade; their diagnostic yield was 6% and 29%, respectively. "Diagnostic" biopsy (20 patients) was carried out when illness persisted for longer than 3 weeks, whereas "therapeutic" biopsy was performed whenever pericardiocentesis failed to relieve tamponade; their diagnostic yield was 5% and 54%, respectively. The diagnostic yield difference between "diagnostic" and "therapeutic" procedures was significant (p less than 0.001); in contrast, the global diagnostic yield of pericardiocentesis (19%) and biopsy (22%) was similar. At the end of follow-up (1 to 76 months, mean 31 +/- 20), no patient in whom a diagnosis of idiopathic pericarditis had been made showed signs of pericardial disease. It is concluded that a "diagnostic" procedure is not warranted as a routine method, a choice between "therapeutic" pericardiocentesis and biopsy is circumstantial and must be individualized, and only through a systematic approach can a substantial diagnostic yield be reached in primary acute pericardial disease.

In 16 of 177 patients with effusive acute idiopathic pericarditis (10 men, 6 women, mean age 38 years), features of cardiac constriction were detected (by physical examination in 6 patients and by noninvasive recordings in all) between 5 and 30 days after an echocardiogram had shown pericardial effusion, at a time when signs of activity had abated and effusion was already minimal or had altogether disappeared. Cardiac catheterization was performed in 5 patients, showing either overt (3 patients) or occult (2 patients) cardiac constriction. Two patients had clinical signs of cardiac failure. After a mean of 2.7 months, the features of constriction had spontaneously disappeared In all patients in the clinical examination and noninvasive recordings, and remained so In subsequent control studies (mean follow-up 31 months). Repeat cardiac catheterization in the 5 patients in whom it had been previously performed showed normal features both in the basal state and after fluid overload. The results of the present study show that some patients may go through a transient phase of cardiac constriction at the end of the effusive period of acute idiopathic pericarditis. Features of constriction are, in most cases, subtle and can go unrecognized if not specifically sought. However, they may have clinical relevance in some patients. These findings provide insight into the resolution phase of effusive acute idiopathic pericarditis, and an unneccesary pericardiectomy may be avoided.