Diagnosis of increased pulmonary blood flow by suprasternal M-mode echocardiography in atrial septal defect

The right pulmonary artery (PA) was quantitatively assessed by Suprasternal M-mode echocardiography in 25 patients in whom an atrial septal defect (ASD) was suspected clinically. In 10 patients an ASD was excluded (Group 1) and in 15 it was confirmed (Group 2). The smallest diameter of the right PA at end-diastole in Group 1 was 8.8 ± 1.5 mm/m² body surface area and in Group 2 14.8 ± 3.6 mm/m² (p < 0.001). The greatest diameter of the right PA during systole was also much smaller in Group 1 (11.3 ± 1.2 mm/m²) than in Group 2 (17.7 ± 3.5 mm/m²) (p < 0.001). The absolute and percent systolic expansion of the right PA did not differ in the 2 groups (2.7 ± 0.5 mm [29.1 ± 10.8%] in Group 1 and 2.9 ± 0.8 mm [20.8 ± 9.8%] in Group 2). No correlation was found between measured and derived echocardiographic variables of the right PA and the magnitude of the left-to-right shunt. Patients in Group 2, who had an additional pressure elevation in the PA, showed, on average, a larger right PA and a smaller percent systolic expansion. The study demonstrates characteristic alterations in the wall motion pattern of the right PA in patients with ASD, indicating increased pulmonary blood flow.     

Long-term antiarrhythmic therapy with flecainide

The antiarrhythmic efficacy and safety of oral flecainide were assessed during a controlled 2-week and a subsequent 48-week long-term trial. Fifteen patients with frequent (more than 30 per hour) and complex ventricular arrhythmias (Lown grade IVA or IVB) who had been resistant or intolerant to 2 or more antiarrhythmic agents, were included in the study. Antiarrhythmic efficacy was controlled by 24-hour Holter monitoring at 2, 12, 24 and 48 weeks. The administration of 100 to 200 mg flecainide twice daily resulted in more than 90% suppression of VPCs and of complex ventricular arrhythmias in 14 of 15 patients. The minimum effective therapeutic dose could be titrated in 9 of 14 patients to 100 mg twice daily, in 3 of 14 patients to 150 mg twice daily and in 2 of 14 patients to 200 mg twice daily. During this therapy and a mean plasma concentration of 886 +/- 103 ng/ml, PQ and QRS duration, as well as QTc time and JTc interval were not significantly changed. Side effects (gastrointestinal complaints, nausea, obstipation, dizziness, visual disturbances, headache and impaired potency) were seen in 5 of 14 patients after 12 weeks, in 3 of 4 patients after 24 weeks and in only 2 of 14 patients after 48 weeks. Side effects were described as mild and tolerable and did not limit flecainide therapy except in 1 patient, who had discontinued therapy with flecainide after 3 days because of intense gastrointestinal symptoms. In conclusion, flecainide is highly effective and well tolerated in the long-term treatment of serious ventricular arrhythmias.     

Intracoronary thrombolysis in acute myocardial infarction: An attempt to quantitate its effect by comparison of enzymatic estimate of myocardial necrosis with left ventricular ejection fraction

The quantity of myocardium was estimated that can be salvaged by reperfusion of acute transmural myocardial infarction (MI). Serial analysis of serum creatine kinase (CK) activity was carried out in 41 consecutive patients with acute MI who underwent intracoronary thrombolysis. Enzymatic estimate of MI size was calculated using an average (method A) and an individually determined elimination constant (method B). Left ventricular ejection fraction 4 weeks after successful thrombolysis (cineangiogram) correlated inversely with MI size (method A: r = −0.85, method B: r = -0.76; both p < 0.001). Patients with recanalization within 4 hours after the onset of symptoms were assembled in group A₁ (n = 13, early reperfusion), and patients with successful recanalization after 4 hours in group A₂ (n = 16, late reperfusion). Group B consisted of 12 patients without reperfusion. MI size in group A₁ was 21 CK-g-Eq (method A) and 23 CK-g-Eq (method B), in group A₂ 50 CK-g-Eq (method A) and 54 CK-g-Eq (method B), and in group B 73 CK-g-Eq (method A) and 63 CK-g-Eq (method B). Mean values in group A₁ were lower than in group A₂ and group B (p < 0.05). It is concluded that MI size was significantly reduced to about one third after early reperfusion as compared with no reperfusion. In contrast, MI size was not significantly reduced after late reperfusion.     

Intracoronary thrombolysis in acute myocardial infarction: Correlations among serum enzyme,scintigraphic and hemodynamic findings

The effect of early reperfusion after intracoronary infusion of streptokinase in patients with acute myocardial infarction was assessed in 27 patients by serial analysis of serum creatine kinase (CK) activity, thallium-201 scintigraphy (seven pinhole technique) and left ventricular and coronary angiography. Serial serum CK activity determinations were carried out at hourly intervals. Thallium-201 tomographic scintigrams were obtained before and 24 hours after recanalization. The size of the perfusion defect was measured from eight scintigraphic cross sections of the left ventricle. Regional ejection fraction was determined from the left ventricular angiogram before and 4 weeks after recanalization. The results in three groups of patients are presented: group A, 10 patients with successful recanalization and a peak serum CK activity of less than 1,000 U/liter; group B, 9 patients with successful recanalization and a peak serum CK activity of more than 1,000 U/liter and group C, 8 patients with unsuccessful recanalization. Patients in group A showed an increase in CK activity (from 46 to 603 U/liter p < 0.001), a reduction in the thallium perfusion defect (from 115 to 49 °, p < 0.01) and an augmentation of regional ejection fraction (from 24 to 38 percent, p < 0.05). Patients in group B had an increase in serum CK activity (from 46 to 1,562 U/liter, p < 0.001), only a moderate reduction in the thallium perfusion defect (from 141 to 87 °, p < 0.01) and no change in regional ejection fraction (from 25 to 27 percent, p > 0.05). Patients in group C had an increase in serum CK activity (from 43 to 1,756 U/liter, p < 0.001), no change in the thallium perfusion defect (from 145 to 147 °, p > 0.05) and no change in regional ejection fraction (from 32 to 26 percent, p >0.05). Compared with patients in group B, those in group A had a shorter duration of ischemia (3.9 versus 4.8 hours), more frequently adequate collateral supply to the infarcting area before recanalization (40 versus 0 percent of patients) and a smaller area supplied by the occluded vessel (115 versus 141 °). Although all differences were not at the level of significance (p > 0.05), conditions for tolerating ischemia were better in group A than in group B.The study shows that early reperfusion has a beneficial effect on the extent of myocardial necrosis as estimated from serum enzyme determinations, thallium-201 scintigraphy and contrast ventriculography. The beneficial effect depends on the duration of myocardial ischemia and on the blood supply to the ischemic area by collateral vessels.     

Intracoronary thrombolysis in acute myocardial infarction: Duration of ischemia as a major determinant of late results after recanalization

To define the effect of duration of myocardial ischemia on the late results after successful thrombolysis in patients with acute transmural myocardial infarction, data on 39 patients treated with intracoronary infusion of streptokinase were analyzed. Patients with successful recanalization of infarct vessel and a time lag between onset of symptoms and reperfusion less than 4 hours were assembled in group A1 (n = 15) and patients with successful recanalization but a time lag of more than 4 hours (n = 17) in group A2. Group B consisted of 7 patients with unsuccessful thrombolysis. Coronary anatomy, left ventricular volume, ejection fraction and regional ejection fraction of infarct area were determined before and 4 weeks after thrombolysis with cineangiography. Serum creatine kinase activity was serially measured.Before intervention, the groups were comparable with regard to age, Killip class, localization of infarction, incidence of previous infarction, Gensini score of coronary anatomy, left ventricular volume, ejection fraction, regional ejection fraction of infarct area and serum creatine kinase activity. Four weeks after the intervention, patients in group A1 had a higher ejection fraction (59 %) and regional ejection fraction of infarct area (39%) than patients in group A2 (ejection fraction: 49%, p < 0.05; regional ejection fraction: 26%, p < 0.05) and group B (ejection fraction: 44%, p < 0.05; regional ejection fraction: 25%, p = 0.05). Peak serum creatine kinase activity measured during the acute illness was lower in group A1 (764 U/liter) than in group A2 (1,580 U/liter, p < 0.05) and group B (2,106 U/liter, p < 0.05).Thus, contraction of infarct area was improved and enzymatic estimate of infarct size was reduced after early as compared with late reperfusion in patients with acute myocardial infarction.     

Diagnosis of dissecting aortic aneurysm with suprasternal echocardiography

A 33 year old woman with Marfan's syndrome and aortic root dissection was studied with precordial and suprasternal echocardiography. The precordial approach revealed some typical features of aortic root dissection. With suprasternal echocardiography it was possible to visualize the characteristic diagnostic feature of this disease: within the aortic lumen an m-shaped pattern--the aortic intimal flap--moving downward to the posterior aortic wall during systole. The diagnosis was confirmed with aortic cineangiography and intraoperative findings. Thus, suprasternal echocardiography can be a useful method of detecting aortic root dissection, especially in patients with aortic arch dissection alone.     

Metabolites of the aminoacetone pathway in blood after exercise

The following article reports (A) data on glyoxalase I activity in skeletal muscle of untrained men and endurance—trained athletes, and (B) the presence at rest and the rise in blood after exercise of two metabolites of the aminoacetone pathway of amino acid degradation in man. Glyoxalase I showed an average activity of 191 ± 38 U/g wet weight (37°C) in bioptic samples of m.vastus medialis quadricipitis of young adults whereas this was of 235 ± 64 U/g (p < 0.15) in athletes. After an ergometer exercise test with increasing intensity (50 to 400 Watt (W), 3 min-steps) by well trained cyclists, blood L-(+)-lactate increased to 10.12 mmole/liter, whereas methylglyoxal rose by 48.4% and D-(-)-lactate by 70% (resting levels 92 and 110/μmole/liter, respectively). The possible physiologic significance of the assumed aminoacetone pathway was discussed with respect to muscular activity.     

Reduction of creatine kinase and creatine kinase-MB indexes of infarct size by intravenous verapamil

In a prospective, controlled study, 29 patients were randomly allocated to receive intravenous verapamil, 5 to 10 mg/hour, for 2 days starting at a mean of 8 hours after the onset of myocardial infarction. Twenty-five patients received no specific treatment and served as control subjects. Left ventricular (LV) filling pressure in all patients was initially less than 15 mm Hg. Age, infarct localization and hemodynamic values on admission (Swan-Ganz catheter) were comparable in both groups. Maximal creatine kinase (CK) and creatine kinase-MB (CK-MB) values were markedly lower in the verapamil group than in the control group (CK 547 vs 703 U/liter, p less than 0.05; CK-MB 51 vs 68 U/liter, p less than 0.025), as was infarct weight (48 vs 65 g-Eq, p less than 0.03; CK-MB 31 vs 49 g-Eq, p less than 0.005). Arterial blood pressure was 10% lower in the verapamil group than in the control group. Systemic vascular resistance and LV filling pressure remained unchanged. Verapamil reduced myocardial infarction size by about 30% in patients without LV failure and the arterial pressure was reduced.     

Differential effects of sotalol and metoprolol on induction of paroxysmal supraventricular tachycardia

Seventeen patients with recurrent paroxysmal supraventricular tachycardia (SVT) underwent serial electrophysiologic studies to compare the effects of i.v. sotalol (1.5 mg/kg) and i.v. metoprolol (0.15 mg/kg). The plasma concentrations of sotalol (2.1 ±1.1 μg/ml) and metoprolol (67 ± 15 ng/ml) were within the therapeutic range. Before drug administration, sustained SVT could be reproducibly induced in all patients. Sotalol prevented induction of sustained SVT in 10 of 17 patients (59%) and metoprolol in 4 (28%) (p < 0.05). In 6 of 8 patients with atrioventricular (AV) nodal reentrance, the site of action of sotalol was the anterograde or the retrograde limb, reflecting an increase in refractoriness in both pathways of the circus movement. In 4 of 9 patients with AV reentrance, the site of action of sotalol was exclusively the AV nodal pathway; conduction through the extranodal accessory tract appeared to be unchanged, but lts anterograde effective refractory period was prolonged (from 285 ± 25 to 322 ± 28 ms, p <0.001; mean ± Standarddeviation). In the 7 patients in whom sotalol did not prevent sustained SVT, the tachycardia cycle length increased from 347 ± 42 to 392 ± 45 ms (p <0.01). Compared with sotalol, metoprolol had qualitatively similar but quantitatively less potent effects on the AV nodal pathways; however, different from sotalol, metoprolol had no effect on extranodal accessory tracts.The study suggests that at therapeutic plasma concentrations, sotalol would be effective in preventing clinical SVT in a significant proportion of patients refractory to metoprolol; because sotalol not only has β-blocking properties but also results in acute prolongation of the action potential duration, this combination of class II and III activity may contribute to its superior prophylactic efficacy compared with pure β blockade.     

Ventricular arrhythmias before and late after aortic valve replacement

The influence of aortic valve replacement on the incidence of ventricular arrhythmias was studied by 24-hour Holter electrocardiographic monitoring in 45 patients immediately before and 14 ± 7 months after operation. Ventricular arrhythmias were graded according to the Lown criteria. Preoperative left ventricular (LV) ejection fraction (EF) was determined by angiography and postoperative LVEF by gated blood pool scintigraphy. Repetitive ventricular arrhythmias (Lown grade 4A/B) were associated with a reduced LVEF (< 55%) before and after operation. In 24 patients with preoperative normal LVEF (>- 55%) (group A), mean LVEF remained unchanged after operation (72% vs 71 %). Pre- and postoperative ventricular premature complex (VPC) frequency (45 ± 99 vs 39 ± 94 VPC/24 hours and grade (1.3 vs 1.4) were not significantly different. However, in 17 patients with preoperative impaired LVEF (< 55%) (group B, LVEF preoperatively 40 ± 8%) and marked postoperative improvement (> 10%) (LVEF postoperatively 64 ± 7%), mean VPC frequency decreased from 536 to 69 VPCs/24 hours and mean VPC grade was reduced from 3.8 to 1.5. Complex VPCs were found preoperatively in all 17 patients of group B, but in only 5 patients after operation. Four patients had a reduced LVEF preoperatively and it did not improve postoperatively (group C). Postoperative Holter monitoring detected ventricular tachycardia in all 4 patients.This study indicates that repetitive VPCs are infrequent in patients with normal LVEF before and late after aortic valve replacement. In patients with impaired LVEF and complex VPCs preoperatively, the postoperative improvement of LV function is usually accompanied by a reduction of frequent and complex VPCs.     

Effect of successful thrombolytic therapy on right ventricular function in acute inferior wall myocardial infarction

In 19 patients undergoing intracoronary fibrinolytic therapy for acute myocardial infarction, the site of coronary obstruction was in the proximal right coronary artery. Time between onset of symptoms and hospitalization was less than 4 hours. These patients were studied prospectively by radionuclide techniques immediately after admission, 48 hours and 4 weeks after AMI. Right and left ventricular (RV and LV) ejection fractions (EF) were calculated from gated blood pool scintigrams and the size of the LV perfusion defect was assessed by thallium-201 scintigraphy. Before the intervention, RV performance was significantly lower (RVEF 29 +/- 8%) than normal (53 +/- 7%). The size of the LV perfusion defect was relatively small (less than 25% of LV circumference), and as a consequence, LV pump function was only marginally impaired (LVEF 54 +/- 11%). Recanalization of the infarct artery was achieved in 12 patients (group A); in 7 patients the infarct artery remained occluded (group B). Early after the intervention (48 hours), RV performance in group A recovered significantly (RVEF: 30 +/- 9% vs 39 +/- 7%, p less than 0.01), and further improvement was noted at 4 weeks (RVEF 43 +/- 5%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Correlation between myocardial structure and diastolic properties of the heart in chronic aortic valve disease: Effects of corrective surgery

Left ventricular end-diastolic properties were evaluated with cineangiography and pressure measurements before and 6 months after aortic valve replacement with a Björk-Shiley prosthesis in 10 patients with aortic stenosis, 7 patients with mixed aortic valve disease and 7 patients with aortic insufficiency. Mean left atrial pressure, left ventricular end-diastolic pressure, volume and wall thickness were measured, and the stiffness constant K_A and the elastic stiffness E_m were calculated. Myocardial cell diameter and the degree of myocardial fibrosis were determined with morphometric analysis of transmural needle biopsy specimens obtained from the left ventricular free wall at operation. Significant correlations were found between myocardial cell diameter and end-diastolic pressure (r = 0.63), mean left atrial pressure (r = 0.58), end-diastolic wall thickness (r = 0.80), K_A (r = 0.56) and E_m (r = 0.53). However, no significant correlation existed between percent fibrosis and any of these measurements. Before operation, end-diastolic left ventricular pressure, mean left atrial pressure, K_A and E_mwere significantly elevated in aortic stenosis and mixed aortic valve disease but not in aortic insufficiency. After valve replacement clinical improvement was seen in all patients. End-diastolic left ventricular pressure, mean left atrial pressure, enddiastolic volume and E_m decreased and normalized completely in all groups. End-diastolic wall thickness and K_A decreased significantly in aortic stenosis and mixed aortic valve disease (not in aortic insufficiency) but remained moderately elevated. Close correlations were found between end-diastolic wall thickness and K_A (r = 0.78) and between mean left atrial pressure and E_m (r = 0.85).

These results suggest (1) myocardial cell diameter, but not myocardial fibrosis, is a major determinant of end-diastolic properties of the left ventricle in chronic aortic valve disease. (2) Corrective surgery with a Björk-Shiley valve causes normalization of elastic stiffness of the chamber and of mean left atrial pressure, thus explaining the alleviation of congestive symptoms.     

Coronary dilatory capacity in idiopathic dilated cardiomyopathy: Analysis of 16 patients

Hemodynamic function and overall coronary blood flow (argon technique) were measured in 16 patients with idiopathic dilated cardiomyopathy (IDC) and in 12 patients without detectable heart disease (control subjects) referred for precordial pain. In patients with IDC, coronary blood flow was normal at rest (78 ± 17 ml/100 g·min versus 78 ± 9 in control subjects). During maximal inducible coronary vasodilation (dipyridamole, 0.5 mg/kg), coronary blood flow was significantly reduced (142 ± 38 ml/100 g · min versus 301 ± 64 in control subjects; p < 0.001). Consequently, obtainable minimal coronary resistance was increased in IDC (0.54 ± 0.20 mm Hg/ml/100 g · min versus 0.23 ± 0.04 in control subjects; p < 0.001). In patients with IDC, left ventricular (LV) end-diastolic pressure was significantly increased (19 ± 11 mm Hg versus 6 ± 3 in control subjects; p < 0.005), and the LV ejection fraction was diminished (36 ± 11% versus 72 ± 3% in control subjects; p < 0.001). In patients with IDC, LV end-diastolic pressure correlated significantly with the obtained minimal coronary resistance after application of dipyridamole (r = 0.85; p < 0.001). LV catheter biopsy specimens revealed no alterations in myocardial microvasculature. Thus, coronary dilatory capacity is impaired in patients with IDC, due partially to an increase in extravascular component of coronary resistance.     

Coronary collateral vessels: Their significance for left ventricular histologic structure

Whether coronary collateral vessels protect the left ventricular myocardium is unknown. Light microscopic morphometry was carried out on myocardial tissue samples from 56 surgically treated patients with coronary artery disease. Transmural biopsy of the myocardium perfused by the left anterior descending coronary artery was obtained during open heart surgery. In initial reproducibility studies of biopsy samples of 17 patients a sampling error for evaluation of myocardium was defined and differences in transmural fibrosis exceeding ±6.2 percent were considered biologically significant. Stenosis of the left anterior descending artery was determined from preoperative angiography. Group A (control group) comprised patients with less than 75 percent area reduction of the left anterior descending coronary artery (mean ± standard deviation 65 ±10 percent). Patients in group B (more than 95 percent area reduction [mean 99 ± 2 percent] without collateral supply on arteriography) were compared with patients in group C (identical stenosis [mean 99 ± 2 percent] but with collateral supply). Fibrosis averaged 17 percent in group A, 68 percent in group B (p < 0.001 versus group A) and 29 percent in group C (p > 0.05 versus group A, p < 0.001 versus group B). Thus, in severe coronary stenosis myocardium supplied by collateral vessels shows less fibrosis on biopsy sample than does myocardium without collateral supply.     

Estimation of left ventricular myocardial function by the ejection fraction in isolated, chronic, pure aortic regurgitation

In patients with aortic regurgitation (AR), the left ventricular (LV) ejection fraction (EF) may not adequately reflect depressions of myocardial contractility due to decreased aortic impedance. The sensitivity of end-systolic pressure-volume relations and stress-volume relations in detecting myocardial depression in patients with AR was studied. In 12 patients with normal valvular function but with varying LV function (due to coronary heart disease in 9 patients and dilated cardiomyopathy in 3 patients) (group 1), and in 8 patients with AR (group 2), LV angiography was performed before and after sublingual application of isosorbide dinitrate. Heart rate was kept constant by right atrial pacing. In group 1, the slope k of the end-systolic pressure-volume relation was to EF at rest: k = 0.091.e0.051 EF; r = 0.88. In AR, this relation was shifted significantly to the right: k = 0.019.e0.066 EF; r = 0.92. This shift persisted when the end-systolic stress-volume relation instead of the end-systolic pressure-volume relation was calculated. Thus, in patients with AR the end-systolic pressure-volume relation is flatter than that in patients with intact valvular function at a given EF. The same is true for the end-systolic stress-volume relation. The data indicate that EF overestimates myocardial contractility in AR compared with end-systolic pressure-volume or stress-volume relations. This overestimation is probably a result of decreased aortic impedance in AR.     

Regional myocardial function at rest and after rapid ventricular pacing in patients after myocardial revascularization by coronary bypass graft or by collateral vessels.

The relation between the anatomy of the left anterior descending coronary artery and regional myocardlal function was studied at rest and after rapid ventricular pacing in 194 patients with proximal disease of this artery. Sixty patients were restudied 4 months after coronary bypass surgery. All of these patients had a graft to the left anterior descending coronary artery after operation. Twenty-two persons with normal coronary arteriograms served as control subjects. Coronary obstruction was measured with quantitative coronary artertography and was classified as critical stenosis (75 to 99 percent luminal narrowing) or occlusion (100 percent). Regional wall motion was defined by hemiaxls shortening. Four groups were established: group A, obstruction without revascularization; group B, obstruction with revascularization by collateral vessels; group C, obstruction with revascularization by a patent graft; group D, obstruction with revascularization by a stenosed or occluded graft. At rest, regional motion diminished in group A with critical stenosis and further with occlusion (from 39 to 25 percent and to 5 percent, P < 0.001, P < 0.001); in group B, with critical stenosis (from 39 to 24 percent, P < 0.001) but not with occlusion (from 24 to 19 percent, P > 0.05). In contrast, in group C motion remained unchanged (from 39 to 31 percent and to 32 percent, P > 0.05, P > 0.05). After pacing, regional motion became akinetic in groups A and B with critical stenosis and remained unchanged with occlusion. In contrast, in group C wall motion remained normal after pacing with critical stenosis and with occlusion. Results in group D were comparable with those in group B. Ejection fraction showed parallel and left ventricular end-diastolic pressure inverse changes as compared with regional motion.When coronary stenosis progresses to occlusion without revascularization, myocardial contractility becomes depressed at rest and after pacing. Revascularization by collateral vessels preserves resting function in coronary occlusion to some extent but is ineffective after pacing. Successful surgical revascularization prevents loss of function at rest and after pacing in critical stenosis and in occlusion.     

Determinants of the incidence and severity of ventricular arrhythmias in aortic valve disease

The incidence of ventricular arrhythmias in patients with aortic valve disease was investigated. Twenty-four-hour ambulatory electrocardiographic recordings were obtained in 93 patients without coronary artery disease (aortic stenosis [AS], n = 38; combined AS and aortic regurgitation [AR], n = 27; and AR only, n = 28). The arrhythmias were compared with the hemodynamic findings of cardiac catheterization. Ventricular premature beats (VPB) were noted in 78 patients (84%). They were rare (< 100 VPB/22 hours) in 40 patients (43%), moderately frequent (101 to 1,000 VPB/22 hours) in 23 patients (25%), and frequent (> 1,000 VPB/22 hours) in 15 patients (16%). Multiformity was found in 47 (51%), paired VPB in 32 (34%), and ventricular tachycardia in 17 (18%) of the 93 patients studied. The occurrence of ventricular arrhythmia was not related to the type of valve lesion, to the transvalvular gradient in patients with AS, or to the degree of regurgitation in patients with AR. In contrast, the grade of arrhythmia showed a negative correlation with left ventricular ejection fraction (AS, r_s = ?0.58; AS and AR, r_s = ?0.67; AR, r_s = ?0.78; all p < 0.001) and a positive correlation with peak systolic left ventricular wall stress (AS, r_s = 0.56; AS and AR, r_s = 0.56; AR, r_s = 0.57; all p < 0.001). The frequency of VPB also showed a negative correlation with left ventricular ejection fraction (AS, r_s = ?0.63; AS and AR, r_s = ?0.65; AR, r_s = ?0.71; all p < 0.001).This study indicates that ventricular arrhythmias are present in a large number of patients with aortic valve disease. The severity of arrhythmias is strongly influenced by myocardial performance. Thus, severe arrhythmias are frequently a sign of impaired left ventricular function.     

Diagnostic relevance of humoral and cytotoxic immune reactions in primary and secondary dilated cardiomyopathy

Circulating muscle-specific antimyolemmal antibodies (AMLAs) were found in 18 of 61 patients with secondary dilated cardiomyopathy (DC). All 18 patients had clinical or histologic evidence of previous perimyocarditis. AMLAs were found both in patients' serum samples and bound to the sarcolemmal sheath of the autologous myocardial biopsy specimen. Only AMLAs in postmyocardiac DC induced cytolysis of vital cardiocytes in the presence of complement, whereas hepatocytes remained unaffected. Titers of AMLAs correlated with the degree of cardiocytolysis. In contrast, antiinterfibrillary antibodies were found in 49 % patients with primary DC (n = 79) and in 61 % of patients (n = 30) with alcoholic DC. The incidence of antifibrillary antibodies of the antimyosin type was 23 and 24%, respectively. Incidence of both antibodies increased according to the severity assessed by New York Heart Association functional classes. Circulating immune complexes assayed by a new Clq-solid phase fluorometric assay were present in 30% of patients with postmyocarditic DC only. Lymphocyte-mediated cytotoxicity against heterologous cardiac target cells (K-cell activity) was measured in 33% of patients each with primary and secondary alcoholic DC but not postmyocarditic DC. There were no blocking factors in primary but were some in alcoholic heart disease.     

Thrombolysis in acute myocardial infarction: effect of intravenous followed by intracoronary streptokinase application on estimates of infarct size

The effect of pretreatment with intravenous infusion of streptokinase (SK) (16,700 U/min for 90 minutes), started after diagnosis and followed by intracoronary application (2000 U/min) (protocol 1), was assessed retrospectively in 55 consecutive patients with acute transmural myocardial infarction (MI). Another 46 patients with acute MI treated previously by intracoronary thrombolysis served as control subjects (protocol 2). Reperfusion at first coronary injection was observed after pretreatment in 25 patients (45%), but in no control patient (p less than 0.001). Fifteen patients with successful pretreatment (group A), 20 patients with successful treatment according to protocol 2 (group B) and 9 patients with unsuccessful thrombolysis (group C) were restudied after 4 weeks. Data from patients with reinfarction, coronary bypass surgery or percutaneous transluminal coronary angioplasty before restudy were excluded. Thallium-201 scintigraphy was performed before and 24 hours after treatment, serum creatine kinase activity was measured every 8 hours for 3 days and regional ejection fraction (EF) of acute MI was determined before and 4 weeks after treatment. The scintigraphic, enzymatic and hemodynamic data before treatment indicated severe and comparable ischemia among the 3 groups. The thallium-201 perfusion defect decreased in group A (from 41 to 21%, p less than 0.01) and in group B (from 38 to 26%, p less than 0.01), but did not change in group C (from 37 to 31%, difference not significant). Peak serum creatine kinase levels normalized by the perfusion area of acute MI was 20, 33 and 58 U/liter unit in groups A, B and C. The mean values of groups A and C were significantly different (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)