Relief of diastolic cardiac dysfunction after cyclosporine withdrawal in a cardiac transplant recipient.

Severe heart failure developed in a 49-year-old patient 18 months after orthotopic cardiac transplantation. Acute rejection as well as other overt causes of graft failure were excluded. Haemodynamic measurements suggested severe diastolic myocardial dysfunction. Since no other causes of diastolic heart failure were identified, a potential side effect from cyclosporine was considered. Cyclosporine was therefore withdrawn and immunosuppressive treatment was switched to conventional therapy consisting of azathioprine and prednisolone. Withdrawal of cyclosporine was followed by an impressive clinical improvement and by complete haemodynamic normalization. Therefore, in cases of otherwise unexplained graft failure, a potentially reversible side effect from cyclosporine should be taken into consideration.

Hemodynamic and hemorheologic determinants of left atrial spontaneous echo contrast and thrombus formation in patients with idiopathic dilated cardiomyopathy.

The purpose of the present study was to evaluate the specific role of hemorheologic and hemodynamic parameters for spontaneous echo contrast and thrombus formation in vivo. We therefore investigated the association between the presence of left atrial spontaneous echo contrast and thrombus formation by transesophageal echocardiography and multiple clinical, hemodynamic, and hemorheologic parameters in 70 patients with idiopathic dilated cardiomyopathy. Transesophageal echocardiography showed left atrial spontaneous echo contrast and left atrial thrombi in 33% and 19% of patients, respectively. Patients with left atrial spontaneous echo contrast had a lower cardiac index (2.1 +/- 0.9 versus 2.6 +/- 0.9 L/min/m2; p < 0.02), a lower left atrial (21 +/- 8 versus 38 +/- 10 cm/sec; p < 0.001) and left atrial appendage flow velocity (17 +/- 14 versus 39 +/- 13 cm/sec; p < 0.001), a larger left atrial diameter (53 +/- 6 versus 46 +/- 10 mm; p < 0.002), and more often presented with atrial fibrillation (62% versus 32%; p < 0.02). Plasma fibrinogen concentration (4.0 +/- 1.1 versus 3.5 +/- 0.7 gm/L; p < 0.02) and plasma viscosity (1.83 +/- 0.10 versus 1.76 +/- 0.15 mPa.sec; p < 0.05) were higher in patients with spontaneous echo contrast. Multivariate analysis revealed an association between the presence of spontaneous echo contrast and left atrial flow velocity p < 0.0001) and plasma viscosity (p < 0.01). In patients with left atrial (appendage) thrombus or a history of embolism, left atrial appendage flow velocity was lower (15.0 +/- 8.2 versus 29.6 +/- 14.5 cm/sec; p < 0.005) and spontaneous echo contrast was more frequently observed (52% versus 23%; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Different risk factor profiles in young and elderly stroke patients with special reference to cardiac disorders.

The risk factors of ischemic cerebrovascular disorders in 77 young patients (< or = 40 years) were compared to those in 138 older patients (> 40 years). The risk factor profile of patients with juvenile stroke was considerably different from that of older patients. Migrainous headache and mitral valve prolapse occurred more frequently in the younger age group, whereas hypertension, diabetes mellitus, high levels of cholesterol and triglycerides were found more often in older patients with stroke. 65% of the women under the age of 40 took oral contraceptives which compares to the baseline community value of 28% of women in childbearing age in this country. Cardiac disorders such as atrial fibrillation, left ventricular hypertrophy, coronary heart disease including a history of myocardial infarction, as well as mitral valve disease were demonstrated more often in the group of elderly patients. 7 out of 77 younger patients (9.1%), and 59 out of 138 older patients (42.8%) were considered to belong to a group with "high cardiac risk for stroke". The results of this study indicate that electrocardiographic screening is of prime importance for detecting cardiac risk factors. However, echocardiographic examination often yields additional diagnostic information, particularly in younger patients. The conflicting opinions concerning the relevance of certain risk factors for ischemic stroke could partly be explained by the fact that these risk factors are distributed unevenly depending on age.

Significance of left-sided heart disease for the detection of patent foramen ovale by transesophageal contrast echocardiography.

Detection of patent foramen ovale by contrast echocardiography is based on transient inversion (right atrial pressure higher than left atrial pressure) of the interatrial pressure gradient. Therefore, the presence of left-sided heart disease with potential elevation of left atrial pressure might obscure the diagnosis of patent foramen ovale. Accordingly, 150 patients (88 men, 62 women; mean age 51.7 +/- 15.2 years) were evaluated for a patent foramen ovale by transesophageal contrast echocardiography. Additionally, atrial septal motion during normal respiration and during the Valsalva maneuver was analyzed. Patency of the foramen ovale was observed in 20 (27%) of 74 patients without left-sided heart disease and with previous arterial embolism, in none (0%) of 25 patients with left-sided heart disease and embolism, in 7 (39%) of 18 patients without left-sided heart disease and without embolism and in 3 (9%) of 33 patients with left-sided heart disease and without embolism. The detection rate of patent foramen ovale was lower in patients with than without left-sided heart disease (5% vs. 29%, p = 0.0007) but was similar in patients with and without embolism (20% vs. 19.5%, p = NS). Abnormal atrial septal motion was more frequently observed in patients with left-sided heart disease (p = 0.0003) and was inversely correlated to detection of patent foramen ovale (p = 0.0003). Multivariate analysis revealed an independent association between the absence of left-sided heart disease and the detection of patent foramen ovale (p = 0.0003). These data suggest that in patients with left-sided heart disease, patency of the foramen ovale may be missed even by transesophageal contrast echocardiography.

Pacing-induced myocardial ischemia does not affect the endothelial release of coagulant and fibrinolytic factors into the coronary circulation.

The present study addresses the potential effects of pacing-induced myocardial ischemia on the secretion of coagulant and fibrinolytic factors within the coronary circulation. In 6 patients undergoing programmed ventricular stimulation with repeated induction of clinical ventricular tachycardia, the coronary release of tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI) capacity, von Willebrand factor antigen (WF:Ag), and prostacyclin (6-keto-PGF 1a) was measured. Blood samples were collected simultaneously from the ascending aorta and the coronary sinus at baseline and immediately after the induction of ventricular tachycardia. The occurrence of pacing-induced myocardial ischemia was established by myocardial net lactate production. Myocardial ischemia was induced in every patient by repeated pacing trials. Pacing-induced ischemia did not affect the coronary release of any of the above factors. Consequently, there was no alteration of transcardiac gradients of thrombin-antithrombin complexes and D-dimer. The present results indicate that pacing-induced myocardial ischemia does not affect the release of coagulant and fibrinolytic endothelial factors or prostacyclin into the coronary circulation.

Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia.

We studied the prognostic relevance of inducible ventricular tachycardia in 32 patients with dilated cardiomyopathy and spontaneous nonsustained asymptomatic ventricular tachycardia. Programmed ventricular stimulation included basic drive cycle lengths of 600, 500, 430, 370, 330 and 300 msec at single, double, and triple extrastimuli. Ventricular tachycardia (greater than or equal to 6 beats) was initiated in 7 patients (22%), with sustained monomorphic ventricular tachycardia being seen in 4 of them. During median follow-up of 21 months (13-44), 14 patients died. Sudden cardiac death occurred in two of the seven patients with inducible tachycardia and in only one of the 25 patients in whom it was not possible to induce tachycardia. Although patients with inducible tachycardia did not differ clinically from those in whom tachycardia could not be induced, the projected mean survival time was significantly shorter in those with inducible tachycardia (10 months vs. 32 months, P = 0.04). For late sudden cardiac death, the positive predictive value of inducible tachycardia was 28%. The negative predictive value was 96%. We conclude that induction of ventricular tachycardia by programmed stimulation might indicate poorer prognosis in patients with dilated cardiomyopathy.

Electrophysiologic testing after aortic valve replacement in two patients with aortic stenosis and preoperative ventricular fibrillation.

In two patients with severe aortic stenosis successful resuscitation from ventricular fibrillation was documented by Holter recording/ECG monitoring. After aortic valve replacement programmed ventricular stimulation was performed in both patients, but ventricular tachycardia/ventricular fibrillation was not inducible. The patients were left without antiarrhythmic therapy and have been free from cardiac events for 18 and 20 months, respectively. The prognostic value of postoperative electrophysiologic testing after aortic valve replacement in patients with severe aortic stenosis and preoperative resuscitation is discussed.

Combined sotalol and flecainide given at low dosage in patients with the Wolff-Parkinson-White syndrome.

We determined the effects of combined sotalol (160 mg/day) and flecainide (200 mg/day) in 15 patients with the Wolff-Parkinson-White syndrome. After medication given for 3 days, the plasma levels were 0.8 +/- 0.3 micrograms/ml for sotalol and 232 +/- 104 ng/ml for flecainide. Electrophysiologic testing showed complete blockade of the accessory pathway in 4 patients and a decrease in the anterograde conduction capacity by 27% in the remainder. The effect on the accessory pathway was unrelated to the resting conduction properties. Initiation of circus movement tachycardia was prevented in 5 of 11 patients. During a median period of 28 months of follow-up, 87% of patients were either free of tachycardia or satisfactorily improved. No proarrhythmic or adverse drug effects were observed.

Electrophysiologic determinants of recurrent atrial flutter after successful termination by overdrive pacing.

The potential ability of electrophysiologic abnormalities to predict recurrence of atrial flutter was evaluated. Twenty-five patients with chronic atrial flutter resistant to combined digitalis and quinidine therapy were studied electrophysiologically after restoration of sinus rhythm by overdrive pacing or by eventual direct current cardioversion. Recurrence of atrial flutter was observed in 12 patients during a mean follow-up period of 17 months (range 3 to 50). Electrophysiologic testing included programmed high right atrial stimulation at a paced drive cycle length of 600 ms and incremental pacing up to 200-ms paced intervals. When coupling intervals of 90% of the drive cycle length were compared to coupling intervals of 48% of the drive cycle length, the increase in S1A1 interval, defined as the interval between the stimulus artifact and the atrial activation near the atrioventricular junction, was greater in patients with subsequent recurrence of atrial flutter (47 +/- 11 vs 21 +/- 18 ms). Stepwise logistic regression analysis identified the S1A1 increase to be the sole independent predictor of recurrence (p = 0.0082) while previous episodes of atrial flutter or the presence of organic heart disease were identified as dependent variables. Reclassification showed a 91% sensitivity and a 92% specificity. Correct classification was achieved in 92% of patients. The initiation of atrial dysrhythmia had no predictive value. The assessment of the S1A1 interval by programmed atrial stimulation appears helpful in delineating the patient risk of recurrent atrial flutter after termination by overdrive pacing.

Inadvertent catheter-induced right bundle branch block in a patient with preexistent left bundle branch block and recurrent macroreentrant ventricular tachycardia.

This article describes the inadvertent, catheter-induced induction of right bundle branch block resulting not only in transient complete infra-His heart block but also in temporary interruption of the macroreentry circuit of ventricular tachycardia. A patient with preexistent left bundle branch block and spontaneous ventricular tachycardia based upon the bundle branch reentry mechanism underwent electrophysiological testing for the evaluation of sotalol drug efficacy. In search of an optimal His-bundle recording, the manipulation of a 6 Fr quadripolar catheter caused a right bundle branch block, thus advancing the preexistent left bundle branch block to complete heart block. Retrograde ventriculoatrial conduction remained unaffected. The macroreentrant tachycardia with left bundle branch block configuration was no longer inducible. While the patient continued on unchanged sotalol medication (320 mg/d) he required temporary pacing for 16 hours until the block subsided. A subsequent induction attempt demonstrated initiation of the tachycardia. Finally, guided by invasive testing, the patient successfully received amiodarone therapy (300 mg/d). The patient completed an uneventful follow up of 27 months. No progression of conduction delay was observed. This case suggests that the inadvertent induction of right bundle branch block prevents the initiation of ventricular tachycardias relying on bundle branch reentry. Therefore, missed diagnosis or misinterpretation of antiarrhythmic drug efficacy might occur if there is no electrophysiological reevaluation after right bundle branch recovery.

[The effect of concomitant aortic valve insufficiency on the values of Doppler sonographic gradient determination in patients with aortic stenosis]. / Einfluss der begleitenden Aorteninsuffizienz auf das Ergebnis der dopplersonographischen Gradientenbestimmung bei Patienten mit Aortenstenose.

We examined the influence of concomitant significant aortic incompetence (AI) on Doppler-gradient measurements in valvular aortic stenosis (AS) by comparing catheter and Doppler gradients of 51 patients with isolated AS and of 24 patients with additional AI. In patients with additional AI there was a significantly greater overestimation of the peak-to-peak gradient by the maximal instantaneous Doppler gradient (AS + AI: overestimation 31.0 +/- 17.6 mm Hg, AS: overestimation 10.5 +/- 20.2 mm Hg; p less than 0.01) and also by the maximal instantaneous catheter gradient (AS + AI: overestimation 32.8 +/- 11.8 mm Hg, AS: overestimation 20.4 +/- 14.0 mm Hg; p less than 0.01). Comparison of the respective catheter-derived and Doppler-sonographically measured instantaneous and mean gradients showed no differences between the two patient subgroups. Higher instantaneous gradients in patients with additional AI are mainly explained by the lower end-diastolic aortic pressure. However, Doppler-sonographic overestimation of the severity of stenosis in patients with combined AS + AI, due to the sole measurement of the instantaneous gradient in clinical practice, should be of limited importance because in these patients significant AI already sufficiently indicates aortic valve replacement.

Day to day reproducibility of Doppler sonographic measurements in patients with valvular aortic stenosis.

High reproducibility of Doppler gradient measurements is necessary for both the reliable noninvasive assessment of the severity of aortic stenosis and for repeated follow-up examinations in individual patients. We therefore studied day to day reproducibility of Doppler sonographically measured peak pressure drops in 46 patients with valvular aortic stenosis. Clinically stable patients were examined twice within 29 +/- 18.2 days by the same examiner. Peak pressure drop (PPD) and peak flow velocity differed between the two examinations by 8.6 +/- 7.0 (range 0-29) mmHg and by 0.25 +/- 0.18 (range 0-0.7) m/s, respectively. Reproducibility was comparable in patients with excellent, good, and moderate quality examinations, but was lower in the 6 patients with poor quality examination. Variability of PPD, but not of peak flow velocity was higher (p less than 0.05) in patients with severe (PPD greater than 60 mmHg) stenosis. Reproducibility was comparable in patients with or without concomitant aortic incompetence and in patients with normal or reduced left ventricular function. Similar reproducibility was obtained in patients with heart rate changes below or above 10 beats/min between the two examinations. It is concluded that good reproducibility of Doppler measurements in patients with aortic stenosis allows reliable noninvasive assessment of the severity of the stenosis. In follow-up studies of patients with mild to moderate aortic stenosis increases in peak flow velocity in excess of 15% (mean day to day variability +2 SD) are highly indicative of the true progress of the stenosis.

[Electrophysiologic study in patients with syncope of unknown cause]. / Elektrophysiologische Untersuchung bei Patienten mit unklaren Synkopen.

Electrophysiologic studies were performed in 51 patients with syncopes of unexplained origin. 25 patients (49%) had organic heart disease. Electrophysiologic testing included determination of corrected sinus node recovery time, AV-nodal effective refractory period, AH- and HV-intervals, and AV-nodal Wenckebach rate. During programmed right ventricular stimulation, 1-3 premature stimuli were used. 26 patients (53%) had an abnormal outcome that strongly suggested an arrhythmogenic cause of the reported syncopes. In ten patients (20%), corrected sinus node recovery time was prolonged; AV-nodal conduction disturbance was manifest in two patients (4%); reversibility with atropine was shown in one patient. Six patients (12%) had an infrahisian conduction delay with an HV-interval longer than 70 ms. Eight patients (15.6%) had either symptomatic ventricular tachycardias (n = 4), AV-nodal reentry tachycardias (n = 2), or inducible symptomatic rapid atrial fibrillation (n = 2). In one additional patient, ventricular tachycardias could not be reinitiated after ending tricyclic antidepressant drug medication. The diagnostic yield of the electrophysiologic study was not influenced by the presence of organic heart disease. Patients with prolonged corrected sinus node recovery time, prolonged HV-interval, and irreversible AV-conduction delay underwent pacemaker implantation (n = 17). Patients with rapid response to programmed stimulation received antiarrhythmic medication, the efficacy of which was assessed by serial electrophysiologic testing until non-inducibility was obtained. The mean follow-up period was 11 months (1-31 months). Overall 2-year mortality was 17%. In 4/5 patients, death was unrelated to the cause of syncope.(ABSTRACT TRUNCATED AT 250 WORDS)

[Doppler echocardiographic determination of aortic valve gradients]. / Doppler-Echokardiographische Bestimmung des Aortenklappengradienten.

Doppler-echocardiography is the most important non invasive method for the assessment of the severity of aortic stenosis. After measuring the maximal transstenotic flow velocity (= Vmax) the maximal pressure drop between left ventricle and aorta (= maximal instantaneous gradient) can bei calculated according to a simple formula. The accurate determination of Vmax may be difficult and time consuming, however, and when interpreting the Doppler-data it is important to realize that there is always a systematic numerical difference between the instantaneous gradient and those gradients which one usually measures at catheterization (peak to peak and mean gradient respectively). In mixed aortic valve disease the aortic insufficiency will distort the relationship between the various gradients still further. Despite these problems Doppler-echocardiography is extraordinarily useful in quantitating aortic stenosis and obviates the need for catheterization in most patients.

[Sudden cardiac death during long-term ECG monitoring of a patient with aortic stenosis]. / Plötzlicher Herztod im Langzeit-EKG bei einem Patienten mit Aortenstenose.

Sudden cardiac death was documented on a Holter-monitor ECG in a 71-year-old man with known, but unoperated, calcific aortic stenosis (peak transvalvar gradient of 90 mm Hg). The tracing showed the development of a, presumably stress-induced, sinus tachycardia with broad QRSs and rapid transition to ventricular fibrillation. This rarely documented example of cardiac death in a patient with aortic stenosis during long-term ECG monitoring is of special interest because the patient had neither an inverse therapy effect nor impaired left-ventricular function.

Thromboembolism in patients with prosthetic heart valves. An adequately controlled intense anticoagulant therapy and its influence on the occurrence of thromboembolism in relation to valve type.

This study was designed to evaluate the efficacy of carefully controlled treatment with oral anticoagulants in patients with different mechanical heart valve prostheses. One hundred eighty-one patients with various types of prosthetic valves (mitral 89, aortic 87, combined 5) received oral anticoagulation aiming at Thrombotest (TT) values between 5% and 12%. Median follow-up was 46 months; 80.8% of all TT determinations were below 12%. The thromboembolic rate was 0.25%/year in patients with aortic valve replacement (AVR) and 4.87%/year in patients with mitral valve replacement (MVR). There was a strikingly lower incidence of thromboembolism with newer types of valves (Björk-Shiley convex-concave) in the mitral position under exactly the same intensity and stability of anticoagulant treatment. Clinically overt valve occlusion could be almost completely prevented (0.12%/year) in prostheses at both sites. Severe hemorrhage occurred at a rate of 1.71%/year and fatal bleeding at a rate of 0.37%/year. Our results indicate that carefully controlled anticoagulation is effective in the reduction of thromboembolic complications at a reasonable risk of bleeding.