Wolfgang Kasper

Mode of death in idiopathic dilated cardiomyopathy: A multivariate analysis of prognostic determinants

A total of 110 patients with idiopathic dilated cardiomyopathy were followed prospectively for 53 +/- 8 (range 41 to 69) months to determine prognostic factors identifying patients at risk for sudden death or death from congestive heart failure. During the follow-up period 39 patients died, 14 of congestive heart failure and 25 suddenly. The incidence of cardiac death after 1 year was 18%, after 2 years 35%, and after 4 years 39%. Multivariate logistic regression analysis identified four independent prognostic factors: left ventricular ejection fraction, cardiac index, number of ventricular pairs/24 hours, and atrial rhythm (sinus rhythm or atrial fibrillation). With the final model of logistic regression 77 of 88 patients (88%) could be classified correctly as being at risk for death from chronic heart failure or sudden cardiac death. Patients who were likely to die of congestive heart failure were characterized by a markedly impaired left ventricular function (measured in terms of left ventricular ejection fraction, cardiac index, or both) and a low number of pairs/24 hours. The association between frequent complex ventricular arrhythmias and depressed left ventricular function identifies patients who are at risk for sudden death. The presence of atrial fibrillation significantly increases the risk of sudden death and death from congestive heart failure.

Effects of intravenous urokinase versus alteplase on total pulmonary resistance in acute massive pulmonary embolism: A European multicenter double-blind trial

Twelve centers participated in a double-blind study in which 63 patients with angiographically documented acute massive pulmonary embolism were randomly assigned to treatment with either urokinase (4,400 U/kg as an intravenous bolus infusion, then 4,400 U/kg per h over 12 h; n = 29) or alteplase (10 mg as an intravenous bolus infusion, then 90 mg over 2 h) followed by heparin (n = 34). The primary objective was to compare the resolution of pulmonary embolism as judged by the change in total pulmonary resistance over the initial 2 h. Further objectives were to evaluate the changes in total pulmonary resistance over the next 10 h and the degree of angiographic resolution at 12 to 18 h. At 2 h, total pulmonary resistance decreased by 18 +/- 22% in the urokinase group and by 36 +/- 17% in the alteplase group (p = 0.0009). Continuous monitoring of pulmonary artery mean pressure, cardiac index and total pulmonary resistance revealed that these variables improved faster in the alteplase group, with consistently significant intergroup differences from 30 min up to 3 to 4 h. After 12 h, the decrease in total pulmonary resistance was 53 +/- 19% in the urokinase group compared with 48 +/- 17% in the alteplase group and the reduction in the angiographic severity score was 30 +/- 25% compared with 24 +/- 18%, respectively, with no significant intergroup differences. Bleeding was equally frequent in the two treatment groups, except that more urokinase-treated patients experienced hematomas at puncture sites.

Analysis of creatine kinase, CK-MB, myoglobin, and troponin T time-activity curves for early assessment of coronary artery reperfusion after intravenous thrombolysis.

BackgroundThrombolysis has become the standard therapeutic approach in patients with acute myocardial infarction. To identify patients who may benefit from early invasive procedures, reliable noninvasive assessment of success or failure of thrombolytic therapy is mandatory. Methods and ResultsIn a prospective study in 63 consecutive patients undergoing thrombolysis for their first myocardial infarction, serial measurements of creatine kinase (CK), its isoenzyme CK-MB, myoglobin, and troponin T were done to determine their value for noninvasive prediction of coronary artery patency. Blood samples were drawn every 15 minutes during the first 90 minutes, every 30 minutes during the first 4 hours, every 4 hours during the first 24 hours, and every 8 hours during the first 72 hours. The perfusion status of the infarct-related artery was assessed angiographically 90 minutes after initiation of thrombolysis. For each marker, time to its peak concentration and its early initial slope (start of thrombolysis to 90 minutes thereafter) were determined. Areas under receiver operator characteristic (ROC) curves were 0.83, 0.76, 0.82, and 0.80 for maxima of CK, CK-MB, myoglobin, and troponin T, respectively (p=NS by univariate Z test). The corresponding values for early slopes of CK, CK-MB, myoglobin, and troponin T were 0.79, 0.82, 0.89, and 0.80 (p =0.23 for comparison between myoglobin and CK-MB;p=0.07 between myoglobin and CK). Sensitivity, specificity, and positive and negative predictive values regarding noninvasive prediction of coronary artery patency after 90 minutes were 80% 82%, 95%, and 61% for time to CK maximum; 91%, 77%, 91%, and 77% for time to myoglobin maximum; 87%, 71%, 89%, and 67% for early CK slope; and 94%, 88%, 94%, and 82% for myoglobin slope, respectively. When myoglobin slope was assessed together with other clinical reperfusion markers (resolution of chest pain or ST segment elevation, occurrence of reperfusion arrhythmias) by logistic regression analysis, only the myoglobin slope was an independent predictor of coronary artery patency (p<0.0001). ConclusionsWith regard to noninvasive prediction of coronary artery patency after thrombolytic therapy, measurement of the early initial slopes of the serum markers within only 90 minutes after the initiation of therapy is as accurate as the determination of the time to their peak concentration. Compared with the other markers examined, myoglobin appears to have advantages because of its earlier rise, yielding a better negative predictive value and a higher area under the ROC curve for determination of its early initial slopes.

Determinants of prognosis in idiopathic dilated cardiomyopathy as determined by programmed electrical stimulation.

The incidence and prognostic significance of electrically induced ventricular arrhythmias were prospectively assessed in 42 patients with idiopathic dilated cardiomyopathy. All patients underwent 24-hour, long-term electrocardiographic (Holter) monitoring and 30 were analyzed by a signal-averaging vectorcardiographic procedure at entry into the study. Their response to programmed electrical stimulation during basic right ventricular pacing was investigated using 1 and 2 ventricular extrastimuli. A monomorphic tachycardia was not induced in any patient. In 36 patients (86%) polymorphic ventricular arrhythmias were initiated. Three or more induced consecutive ventricular premature complexes occurred in 9 patients (21%), nonsustained polymorphic ventricular tachycardia in 2 (4.8%) and ventricular fibrillation in 1 patient (2.4%). There was no association between electrically induced polymorphic ventricular arrhythmias and the degree of impairment of left ventricular function. Furthermore, the incidence of induced ventricular arrhythmias was not related to the Lown grade or to the total number of ventricular premature complexes during Holter monitoring. A late potential was detected by the averaged vectorcardiogram in only 1 of the 30 patients. During follow-up (mean 16 +/- 7 months) 7 patients died, 5 from chronic congestive heart failure and 2 from sudden cardiac death. No patient had an electrically induced arrhythmia of 3 or more ventricular premature complexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Patent foramen ovale in patients with haemodynamically significant pulmonary embolism

The prevalence of a patent foramen ovale is about 1 in 4. In cases with venous thromboembolism and raised right heart pressures, a patent foramen ovale may permit paradoxical emboli, which could complicate the course of patients with pulmonary embolism. Echocardiography enables detection of a patent foramen ovale in life. We have studied 85 patients who presented with haemodynamically significant pulmonary embolism as judged by clinical, echocardiographic, or haemodynamic indices and who had an echocardiographic evaluation for patent foramen ovale. 33 patients (39%) had a patent foramen ovale. Clinical symptoms suggestive of paradoxical embolism were more likely in patients with than in those without a patent foramen ovale (39% vs 6%, p = 0.00034), with new neurological deficits occurring in 11 patients (9 vs 2, p = 0.005) and a vascular occlusion in 8 (7 vs 1, p = 0.0096). Arterial oxygen tension was lower in patients with a patent foramen ovale (mean 55 [SD 14] vs 62 [16] mm Hg, p = 0.038). Mortality was not different between the two groups (27% vs 19%). Cardiopulmonary complications in terms of resuscitation, intubation, or the use of catecholamines were more frequently observed in patients with a patent foramen ovale (48% vs 23%, p = 0.028). Patients with a patent foramen ovale and haemodynamically significant pulmonary embolism are more likely to have arterial hypoxaemia and vascular occlusions, possibly due to paradoxical emboli.

Comparison of alteplase versus heparin for resolution of major pulmonary embolism

Complete resolution of major pulmonary embolism (PE) treated with heparin alone can often take > 3 weeks. Thrombolytic agents effectively resolve pulmonary artery thrombi within a few hours. However, the effect of the 2 types of treatment on recovery of right ventricular function has not yet been followed for periods of > 24 hours. We prospectively examined 40 consecutive patients with documented major PE (symptoms being present for < or = 8 weeks). After diagnosis, 27 patients (68%) were treated with alteplase plus heparin and 13 (32%) with heparin alone. There was no significant difference between the 2 groups with regard to baseline parameters. At 12 hours, systolic pulmonary artery pressure decreased from 56 +/- 20 to 37 +/- 21 mm Hg in the alteplase group, and from 50 +/- 11 to 46 +/- 12 mm Hg in the heparin group (significantly more; p = 0.016). On echocardiographic follow-up, a decrease in end-diastolic dimensions of the right ventricle and an increase in left ventricular dimensions was significantly more pronounced in the alteplase group (p <0.001 and p = 0.05, respectively). The incidence of right ventricular dilation and paradoxical septal wall motion decreased significantly only in the thrombolyis group. However, at 1-week follow-up, no difference was seen between the 2 groups regarding the overall change in right or left ventricular dimensions or the final values of other echocardiographic parameters. Thus, echocardiography is particularly useful for hemodynamic follow-up of major PE. Thrombolysis may rapidly reduce pulmonary artery pressure, but resolution of right ventricular pressure overload also occurs within 1 week in patients treated with heparin alone.

Echocardiographic evaluation of patients with clinically suspected arterial emboli.

153 patients (mean age 42 years, range 16-60) who had arterial embolic events were examined prospectively by transthoracic and transoesophageal echocardiography. Patients older than 60 years and those with evidence of extracranial carotid artery occlusive disease were excluded. 84 patients had a cerebral ischaemic event, 50 patients had embolic events in an abdominal organ or limb, and 19 patients had acute retinal ischaemia. The transthoracic echocardiographic examination was normal in 92 patients (60%), whereas only 65 patients (42%) had normal findings after both transthoracic and transoesophageal examination (p less than 0.005). Intracardiac masses, including valvular vegetations, were found in 39 patients (25%), including 27% of patients with cerebral embolism and 32% of these with peripheral embolism, but in none of the patients with retinal ischaemia (p less than 0.001). 47 patients (31%) had valvular disease, 10 (7%) had wall motion abnormalities, 23 (15%) had abnormalities of the interatrial septum, and 9 patients (6%) had diseases of the thoracic aorta. Cardiovascular abnormalities were frequently found by echocardiography in patients with arterial emboli. The transesophageal technique significantly increased the chance of detecting such abnormalities, especially intracardiac masses.

Risk of transesophageal echocardiography in awake patients with cardiac diseases

Abstract Recent studies described the diagnostic value of transesophageal echocardiography in patients with different diseases of the heart and the thoracic aorta.1–8 However, the risk and potential complications of the transesophageal approach are still under discussion. Schlueter et al6 reported no major side effects during the transesophageal approach in 300 consecutive patients. In accordance with these results, Engberding et al7 also observed no complications using the transesophageal technique in patients with aortic dissection or aortic aneurysm. More recently and in a similar patient population, Erbel et al8 described a 1% incidence of side effects (namely, 1 patient with an attack of asthma and another who experienced a transient atrioventricular heart block). In a prospective study in 54 consecutive patients with different heart diseases undergoing transesophageal echocardiography, we evaluated the presence and severity of “side effects” such as cardiac arrhythmias, marked changes in blood pressure or heart rate and evidence of myocardial ischemia during the diagnostic procedure.

Determination of aortic valve orifice area in aortic valve stenosis by two-dimensional transesophageal echocardiography

Two-dimensional transesophageal echocardiography was used to measure aortic valve orifice area in 24 patients with aortic valve stenosis (AS) and 15 patients without aortic valve disease. Using transesophageal echocardiography, orifice area could be measured in 20 of 24 patients with AS. With transthoracic echocardiography, orifice area could be determined in only 2 of 24 patients. In patients with AS, orifice area determined by transesophageal echocardiography was 0.75 +/- 0.34 cm2 and that calculated with Gorlins formula was 0.75 +/- 0.32 cm2. In normal aortic valves, orifice area was 3.9 +/- 1.2 cm2 by transesophageal echocardiography. A good correlation was demonstrated between aortic valve orifice area determined using transesophageal echocardiography and calculated orifice area using Gorlins formula in patients with AS: r = 0.92, standard error of estimate = 0.14 cm2. The absolute difference between orifice area measured with both methods ranged from 0.0 to 0.4 cm2 (mean 0.09 +/- 0.1). In 4 patients orifice area could not be determined with transesophageal echocardiography. The orifice could not be identified in 2 patients because an appropriate cross-sectional view of the aortic valve could not be achieved and in 2 patients with pinhole stenosis (aortic valve orifice area 0.3 cm2). These data show that aortic valve orifice area can be measured reliably using 2-dimensional transesophageal echocardiography.

Mobile thrombi in atherosclerotic lesions of the thoracic aorta : the diagnostic impact of transesophageal echocardiography

tected in 10 of 36 patients. There were no episodes of ST segment change documented post PTCA. This, however, may have been influenced by their practice of continuing nitrates post PTCA. Gohlke et al5 examined 94 patients 3 to 8 days pre PTCA and again 3 to 8 days post PTCA. Before PTCA 34 patients (36%) had ,102 ischemic episodes, with a total ischemic time of 2486 minutes. Following PTCA the total number of ischemic episodes was reduced to 51, and the total ischemic time was reduced to 1470 minutes. The time periods of ST’segment monitoring used in these other studies were less stringent and not as extensive as in our study, and importantly, in none of these studies were the patients divided according to their angina status. The continuing ischemia post PTCA that we have observed may be the result of an increase in coronary artery tone following PTCA or caused, by platelet emboli arising from the site of dilatation, or the result of failure of the autoregulatory mechanism of the arteriolar circulation, In conclusion, in this selected group of patients the ischemic burden was unchanged in those with stable angina at 48 to 96 hours post PTCA, but was largely abolished in those with unstable angina. These findings suggest a dynamic process post angioplasty that results in continuing myocardial ischemia following successful coronary angioplasty, which was more prolonged in patients with stable angina.