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Subclavian artery stenosis is an infrequently recognized cause of left-sided chest and arm pain that can mimic the signs and symptoms of angina pectoris. In addition, more proximal subclavian artery stenoses can be associated with cerebrovascular symptoms in the "subclavian steal syndrome." This article reviews the clinical experience in four patients who presented with different manifestations of subclavian artery stenosis and who were all successfully treated by percutaneous angioplasty. Their clinical presentation, angiographic findings, and post-angioplasty results are documented. In conclusion, it is felt that nonsurgical correction of critical subclavian artery stenosis, using current angioplasty techniques, is the preferred method of treatment.

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The costs and clinical results of a thrombolytic therapy protocol using intravenous (IV) streptokinase in small community hospitals prior to emergency transfer for cardiac catheterization for possible percutaneous transluminal coronary angioplasty (PTCA) were prospectively studied in 56 patients with an acute myocardial infarction [Tulsa Heart Center-Myocardial Infarction Study Team (THC-MIST) protocol]. Findings were compared to those for 53 similar patients receiving "conventional therapy" during the same study period. The reperfusion rate for IV streptokinase was 63%. Additional emergency PTCA yielded a total reperfusion rate of 95%. Despite emergency cardiac catheterization for all THC-MIST patients, average hospital charges were not significantly different between the two groups ($20,495 vs. $20,722; THC-MIST vs. conventional therapy, respectively). Total charges (hospital plus physician fees) were also not significantly different ($22,986 vs. $22,400; THC-MIST vs. conventional therapy, respectively). Intensive care unit (ICU) days and total hospital stays were significantly less for THC-MIST patients (3.1 vs. 5.8 ICU days, p less than 0.05 and 8.8 vs. 12.4 hospital days, p less than 0.05; THC-MIST vs. conventional therapy, respectively). Thus initiation of IV streptokinase in community hospitals for acute myocardial infarction with subsequent transfer for possible PTCA can yield high reperfusion rates without significantly increasing health care costs.

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The recent establishment of a firm therapeutic role for reperfusion in acute myocardial infarction has stimulated interest in the development of more ideal thrombolytic agents. Anisoylated plasminogen streptokinase activator complex (APSAC) is a new plasminogen activator possessing properties that are promising for intravenous thrombolytic application in acute myocardial infarction. To assess the reperfusion potential of intravenous APSAC, a multi-center, angiographically controlled reperfusion trial was performed. An approved thrombolytic regimen of intracoronary streptokinase served as a control. Consenting patients with clinical and electrocardiographic signs of acute myocardial infarction were studied angiographically and 240 qualifying patients with documented coronary occlusion (flow grade 0 or 1) were randomized to treatment in less than 6 h of symptom onset (mean 3.4 h, range 0.4 to 6.0) with either intravenous APSAC (30 U in 2 to 4 min) or intracoronary streptokinase (160,000 U over 60 min). Both groups also received heparin for greater than or equal to 24 h. Reperfusion was evaluated angiographically over 90 min and success was defined as advancement of grade 0 or 1 to grade 2 or 3 flow. Rates of reperfusion for the two treatment regimens were 51% (59 of 115) at 90 min after intravenous APSAC and 60% (67 of 111) after 60 min of intracoronary streptokinase (p less than or equal to 0.18). Reperfusion at any time within the 90 min was observed in 55 and 64%, respectively (p less than or equal to 0.16). Time to reperfusion occurred at 43 +/- 23 min after intravenous and 31 +/- 17 min after intracoronary therapy. The success of intravenous therapy was dependent on the time to treatment: 60% of APSAC patients treated within 4 h exhibited reperfusion compared with 33% of those treated after 4 h (p less than or equal to 0.01). Reperfusion rates were also dependent on initial flow grade (p less than or equal to 0.0001): 48% (81 of 168) for grade 0 (APSAC = 43%, streptokinase = 54%), but 78% for grade 1 (APSAC = 78%, streptokinase = 77%). APSAC given as a rapid injection was generally well tolerated, although the median change in blood pressure at 2 to 4 min was greater after APSAC than after streptokinase (-10 versus -5 mm Hg). Mean plasma fibrogen levels fell more at 90 min after the sixfold higher dose of APSAC than after streptokinase (to 32 versus 64% of control). Reported bleeding events were more frequent after APSAC but occurred primarily at the site of catheter insertion and no event was intracranial.(ABSTRACT TRUNCATED AT 400 WORDS)

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We report two septic-shock patients who had ECG and echocardiographic changes consistent with myocardial infarction but no evidence of coronary artery disease or myocardial injury at autopsy. The segmental myocardial dysfunction completely resolved in one patient. Because septic shock can cause segmental myocardial dyskinesis, ECG and echocardiographic data may be misleading and should be interpreted cautiously.

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An unusually large family of European descent was afflicted over four generations by an automaticity and conduction disorder with an associated dilated cardiomyopathy of variable expression. Ten living members affected with the disorder and three presumed affected but dead members were identified. Typically, the disorder presented as a sinoatrial bradyarrhythmia/tachyarrhythmia syndrome, followed by atrial enlargement and, variably, ventricular enlargement and dysfunction. Three family members required pacemaker implantation. Longevity did not seem to be greatly affected, but the demonstrated potential for embolic cerebrovascular events stresses an associated morbidity. The familial incidence was best explained by autosomal dominant inheritance with incomplete penetrance (greater in males and usually occurring first in adolescence) and variable expressivity. The large size of the family, frequency and profile of disease manifestations and disease tracking through at least four generations are unusual features of the familial disease described.

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Because of the uncertainty as to the extent to which cardiac size is determined by exercise training vs genetic endowment, this study investigated familial (genetic plus common family environment) vs nonfamilial influences on cardiac size. College-age monozygotic twins (group 1, 31 sets), dizygotic twins (group 2, 10 sets), siblings of like sex (group 3, six sets), and nonrelated subjects (group 4, 15 sets) underwent echocardiographic and electrocardiographic tests, measurement of maximum oxygen uptake (VO2max), and evaluation of pulmonary and body composition; mean intrapair differences of the four groups were compared. Mean intrapair differences in cardiac size varied as much for subjects in group 1 as for those in groups 2 and 3. However, subjects in groups 1, 2, and 3 had less variation (p less than .05) than those in group 4. After the initial testing, 14 pairs of monozygotic twins, five sets of dizygotic twins, and six sets of siblings underwent 14 weeks of exercise training (both members participated) and all tests were repeated. After exercise training, subjects in group 1 still had as much intrapair variability in cardiac size as those in groups 2 and 3. The data suggest cultural familial influences are more important in determining cardiac size than nonfamilial influences or even genetic influences alone.

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Intracoronary streptokinase (SK) may have beneficial effects on the in-hospital course of acute myocardial infarction (MI), but long-term outcome is unknown. We evaluated the outpatient course of 50 MI patients, randomly treated with either SK (n = 24) or standard therapy (n = 26), who presented within 2.7 +/- 0.7 hours of symptoms. Coronary reperfusion occurred in 19 (79%) SK patients. Survivors were followed for a mean of 18.7 months (range 11 to 28.5); information was current in 48 patients (96%). Both groups received antiplatelet therapy for 3 months. A total of five deaths occurred in the control group and two in the SK group, including one posthospital death in each. Nonfatal MIs totaled five in control patients and three in SK patients, including five posthospital MIs (three control, one SK). Differences in major events (death or nonfatal MI) favoring SK did not quite reach statistical significance (10 control vs 5 SK). Bypass surgery was performed in seven SK and four control patients (NS). Angina occurred in more control (15) than SK (six) patients (p less than 0.01), and more control patients used long-acting nitrates (14 control, three SK; p less than 0.01). Palpitations were noted by nine control and one SK patient (p less than 0.01), and documented late arrhythmias were present in four control patients and no SK survivors (p less than 0.05). Symptoms suggestive of heart failure were present in seven control and one SK patient (p less than 0.01); two control patients were hospitalized for failure. Use of beta blockers, calcium channel blockers, and other cardiac medications did not differ.(ABSTRACT TRUNCATED AT 250 WORDS)

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The clinical effects of intravenous streptokinase in patients with acute myocardial infarction were compared with those of intracoronary streptokinase in a randomized, prospective study. Comparisons were also made with a historical control group. Fifty patients were entered into the study at 2.4 +/- 1.2 hr after onset of pain, and 27 were assigned to intravenous and 23 to intracoronary therapy. The doses of streptokinase averaged 212,000 U ic and 845,000 U iv (0.75 X 10(6) U/5 hr, n = 14 or 10(6) U/1 hr, n = 13). Results of studies of the two intravenous dosage schedules were similar and so were combined. Streptokinase was administered at 2.8 +/- 1.0 hr after onset of pain in the intravenous and at 4.3 +/- 1.4 hr in the intracoronary drug group (p less than .001). Convalescent (day 10) radionuclide ejection fractions were 54 +/- 14% for the intravenous and 50 +/- 16% for the intracoronary drug group. Change in ejection fraction from day 1 to 10 tended to be greater after intravenous drug: 5.1% (p less than .08) vs 1.2% (NS). Semiquantitative regional wall motion indexes in the infarct zone showed significant and similar modest improvement from admission to day 10 in both groups (p less than .02). Accelerated enzyme-release kinetics were noted after both therapies. Times of peak enzyme levels for patients on intravenous and intracoronary drug were, respectively, 12.5 +/- 5.0 and 11.5 +/- 4.3 hr for creatine kinase MB isoenzyme and 31.7 +/- 11.8 and 28.1 +/- 12.7 hr for lactic dehydrogenase (LDH). Peak LDH-1 level was lower in patients receiving intravenous drug than in the historical control group (p less than .05). Electrocardiographically summed ST segments diminished rapidly after therapy in both groups; Q wave development was similar and overall R wave loss was equivalent and less extensive compared with in historical control subjects. Infarct pain requiring morphine was diminished similarly in both treatment groups. Incidence of early arrhythmias and heart failure also did not differ. Posttherapy ischemic events and early surgery tended to be more common in the intracoronary group and bleeding was more common in the intravenous group. Intravenous drug did not decrease early hospital mortality (intravenous drug = 5, historical control = 4, intracoronary drug = 1); the differences in this parameter among groups were not significant. At convalescent angiographic evaluation, anterograde perfusion was present in 73% of those receiving intravenous and 76% of those receiving intracoronary drug.(ABSTRACT TRUNCATED AT 400 WORDS)

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To define normal criteria of size and dynamics of the inferior vena cava (IVC) and its clinical value in assessing right-sided cardiac function, 2-dimensional (2-D) and M-mode echocardiography (echo) were performed in 175 subjects, who were classified into 3 groups: group 1-80 normal subjects; group IIA--65 patients with documented right-sided cardiac disease, and group IIB--30 patients with cardiac disease but no right-sided abnormality. The IVC was adequately imaged in 175 of 185 subjects (95%). There was good correlation between M-mode and 2-D echo (r = 0.84) and long- and short-axis (r = 0.88) measurements. The IVC diameter during expiration was: group 1-9 to 28 mm (mean 18.2 +/- 4.6); group IIA--15 to 40 mm (mean 23.1 +/- 4.8) and group IIB-8-24 mm (mean 15.6 +/- 3.7). Collapsibility index (inspiratory decrease in diameter) was: group I-37 to 100% (mean 55.8 +/- 15.9); group IIA--0 to 39% (mean 13.5 +/- 10.5); and group IIB--44 to 100% (mean 60.4 +/- 13.1). A and V waves could be measured in 120 of 151 cases (79%). Both A and V waves were less than 125% of its diameter in group I. The A wave was absent in 34 patients; 30 (88%) were in atrial fibrillation. Among 8 patients with tricuspid regurgitation, 5 (63%) had V waves greater than 125%. There was no correlation between diameter or collapsibility index and age, sex, rhythm or body surface area.(ABSTRACT TRUNCATED AT 250 WORDS)

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Study of 16 normal and 33 flail mitral valves provides evidence of the active participation of chordae tendineae in mitral valve opening. The normal valves have straight chordae at all phases of opening. During isovolumic relaxation and progressive opening phases, the smooth configuration of the mid-anterior mitral leaflet is broken by a sharp outward "tenting." This tenting is localized at chordal insertions, reflecting significant tension at these points. Flail mitral valves allow comparison of opening motion between mitral segments with normal chordal attachment and flail segments without chordal support. Posterior flail leaflets demonstrate delay in initiation of opening motion relative to the normal anterior leaflet. The most dramatic examples of this delay reveal a maximal opening excursion of the anterior leaflet before the flail posterior leaflet initiates opening motion. The untethered free margins of opening flail anterior leaflets produce the appearance of the flail segment trailing the body of the anterior leaflet with a sharp break in leaflet contour between the supported and unsupported segments. These configurational expressions of mitral valve opening are inconsistent with a passive hemogenic mechanism. They support an active myogenic process mediated through direct traction on the valve by the chordae tendineae.

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Twelve electrocardiographic criteria, based on various combinations of Q wave morphology in leads II and aVF, were tested in 235 cases for their diagnostic value in detecting inferoposterior wall motion abnormality (presumably reflecting infarction in the area) as demonstrated on left ventriculogram. The most reliable indicator of inferoposterior wall motion abnormality was found to to a QR complex with a Q wave width greater than or equal to .03 or greater than or equal to .04 sec associated with a Q/R ratio greater than .25. Using as criterion a QR complex with a Q wave width greater than or equal to .04 sec and a Q/R ratio greater than .25, the sensitivity was 41.9% in the cases with akinetic-dyskinetic wall motion and 3.7% in the cases with hypokinesis with an associated specificity of 100%. By lowering the Q wave duration to greater than or equal to .03 sec, the sensitivity increased to 51.6% and 9.3%, respectively, while retaining a very high specificity (96%). The exclusion of cases with a Q and R of less than 5 mm markedly lowered the sensitivity with a negligible increase in specificity. QS complexes in leads II or aVF were not found to be reliable indicators of inferoposterior wall motion abnormality.

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Fifty patients with acute myocardial infarction were randomly assigned to receive either intracoronary streptokinase or standard (control) therapy within about three hours after the onset of pain. Coronary perfusion was reestablished in 19 of 24 patients receiving streptokinase. Streptokinase alleviated pain (as indicated by differences in subsequent morphine use). The Killip class was significantly improved after therapy with streptokinase, as were changes in radionuclide ejection fraction between Days 1 and 10 in surviving patients (+3.9 vs. -3.0 per cent, P less than 0.01). The echocardiographic wall-motion index also showed greater improvement after streptokinase treatment (P less than 0.01). Streptokinase therapy was associated with rapid evolution of electrocardiographic changes, which were essentially complete within three hours after therapy, but loss of R waves, ST elevation, and development of Q waves in the convalescent period were greater in the control group (P less than 0.01). The time required to reach peak plasma enzyme concentrations was significantly shorter after streptokinase. The incidence of early and late ventricular arrhythmias was not affected by treatment. We conclude that intracoronary streptokinase appears to have a beneficial effect on the early course of acute myocardial infarction.

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Thirty-two consecutive patients referred to our institution for evaluation of rheumatic mitral stenosis were studied with M-mode echocardiography (M-mode E), two dimensional echocardiography (2DE), and cardiac catheterization. Twenty-three of these patients underwent mitral valve surgery, 11 requiring mitral valve replacement, and 12 requiring open mitral commissurotomy. Clinical and noninvasive parameters were assessed in order to predict catheterization-determined mitral valve areas as calculated by the Gorlin formula, and to predict the choice of operation in patients selected for surgery. For the prediction of valvular area, 2DE planimetry correlated highly (r = 0.89, p less than 0.01) with Gorlin formula results. The presence or absence of pericardial effusion, the anterior-posterior valve leaflet separation (M-mode E), and the left atrium-aortic index (2DE) correlated poorly with the degree of mitral stenosis as determined by the Gorlin formula. The most useful predictors of type of mitral surgery were age over 50 years, 2DE valve classification, the presence or absence of calcium at fluoroscopy, and degree of anterior leaflet-septal separation (M-mode E).

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The ability of two-dimensional apex echocardiography to evaluate right ventricular and right atrial size was evaluated in 43 normal children and compared with 20 patients with a secundum atrial septal defect. From the apical four chamber view, the long axis length and short axis diameter of the right ventricle and right atrium were measured. The end-diastolic area of the right ventricle and end-systolic area of the right atrium were determined by planimetry. These data were indexed for body surface area. When compared with normal subjects, the area index of the right atrium and right ventricle were enlarged significantly in patients with a secundum atrial septal defect (p less than 0.001 and p less than 0.001, respectively). Mean values for the short axis dimension of the right ventricle and for the short axis and long axis diameter of the right atrium were greater in atrial septal defect patients than in normal subjects (p less than 0.001 for all). However, when both groups were compared, considerable overlap existed between the dimension measurements. Right ventricular long axis length failed to separate the two groups. Thus, two-dimensional apex echocardiography provides a noninvasive means of assessing right ventricular and right atrial size in children with an atrial septal defect.

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In an attempt to formulate a reliable noninvasive method of detecting segmental wall motion disturbances, we examined 25 patients with coronary artery disease by two-dimensional echocardiography (2-DE), standard 12-lead electrocardiography (ECG), and biplane left ventriculography. The 2-DE technic predicted qualitative wall motion abnormalities as defined by ventriculography with a sensitivity of 88% and a specificity of 86%. The ECG (Q waves) predicted segmental wall motion disturbances with only 50% and 51% sensitivity and specificity, respectively. Extrapolating the advantages of 2-DE to the assessment of global myocardial function, left ventricular wall motion index (LVWMI) and E-point septal separation (EPSS) by 2-DE were correlated with left ventriculographic ejection fractions; r values were high (.73 and -.76, respectively) in both instances. Thus, 2-DE provides a reliable noninvasive technic by which both regional and global myocardial wall motion disturbances can be assessed. Unlike previous noninvasive methods, the 2-DE results compared very favorably with those of biplane left ventriculography.

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Regional myocardial function and blood flow were determined for 48 hours after permanent occlusion of the left circumflex coronary artery in conscious swine. Systolic wall thickening and end-diastolic wall thickness (EDWTh) were correlated with regional myocardial flow (RMBF) at 15 minutes, 24 and 48 hours after occlusion. Both regional function and blood flow were compared with the extent of myocardial necrosis (determined histologically) after 48 hours in functionally distinct zones. Group 1 (control zones) was characterized by increased systolic wall thickening, EDWTh, RMBF and had no necrosis. Group 2 (marginal zones) had depressed systolic wall thickening (35 +/- 3% [mean +/ SEM] of preocclusion level at 48 hours) and RMBF (64 +/- 6% of preocclusion values), transiently decreased EDWTh and 46 +/- 5% necrosis. In Group 3 (ischemic zones), all values were greatly reduced: systolic wall thickening was 3.6 +/- 1.2%, EDWTh 76 +/- 8% and RMBF 25 +/- 9% preocclusion values; necrosis was 90 +/- 5%. Groups 2 and 3 had increased RMBF at 24 and 48 hours from that at 15 minutes after occlusion; however, in neither case was systolic wall thickening greater than that at 15 minutes after occlusion. We conclude that there is close correlation between RMBF, systolic wall thickening and the extent of necrosis present after 48 hours of coronary artery occlusion in the conscious swine; subsequent increases in RMBF to the marginal zone after occlusion are not accompanied by improved regional function.

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Echocardiography was used to diagnose the presence of both Ebstein's anomaly and partial atrioventricular canal in the case of a 20-year-old man who presented for evaluation of supraventricular tachyarrhythmias. The diagnosis was confirmed at surgery with successful surgical repair.

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