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S Hohnloser

Publications and source records attributed to S Hohnloser.

51 records · Page 3Linked to original sources

[Anti-arrhythmia effectiveness and tolerance of retard in comparison with standard mexiletine].

In a controlled randomized cross-over trial, 21 patients with coronary artery disease and frequent ventricular arrhythmias were studied to test the efficacy and tolerance of mexiletine 200 mg t.i.d. in comparison to a released application form of mexiletine perlongettes 360 mg b.i.d. During 24-hour Holter monitoring, all patients but one showed more than 30 ventricular premature beats/h; additionally, in 16 patients, complex ventricular arrhythmias (Lown class IV) were documented. In all patients each medication was given for 5 days. Before treatment and during both medication periods, a 4 days' wash-out period was interposed. Mexiletine and mexiletine perlongettes each resulted in a suppression of ventricular ectopy of more than 84% in 10/21 patients (47%); in two patients the response was different. The mean reduction rate in all patients was 68% for mexiletine and 64% for mexiletine perlongettes. In the responder group, the mean reduction rate amounted to 95% under both medications. Ventricular pairs and tachycardia were reduced by more than 90%. Plasma concentration under mexiletine perlongettes was slightly higher, as compared to the standard form of mexiletine; however, under mexiletine, significant changes of plasma concentration were observed during the day only when the standard form was used. Side effects were observed in 8/21 patients (38% for mexiletine) and in 5/21 patients (24% for mexiletine perlongettes). These were mainly gastrointestinal or neurological, but were mild in all patients and did not necessitate discontinuation of the medication in any patient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Noninvasive evaluation of pulmonary hypertension by quantitative contrast M-mode echocardiography.

Although it has been shown that pulmonary flow velocity can be calculated from contrast M-mode echocardiographic tracings, the clinical value of this noninvasive method has not been established. We used contrast M-mode echocardiography to examine the flow velocity pattern at the pulmonary valve in 30 adults referred for diagnostic cardiac catheterization. In the 15 patients with normal pulmonary artery pressure (PAP) (mean pressure less than or equal to 20 mm Hg), midsystolic pulmonary flow velocity was significantly (p less than 0.001) higher (654 +/- 140 mm/sec) compared to the 15 patients with pulmonary hypertension (342 +/- 85 mm/sec, mean pressure greater than 20 mm Hg). Fourteen of the 15 patients with pulmonary hypertension exhibited an early systolic flow velocity peak, whereas all patients with normal PAP showed a dome-shaped systolic flow velocity profile with maximal flow velocity occurring in midsystole. A significant close correlation was found between the relative early to midsystolic flow velocity change and mean PAP (r = 0.96; p less than 0.001). Thus quantitative contrast M-mode echocardiography reliably differentiates patients with pulmonary hypertension from patients with normal mean PAP. In addition, this technique allows a noninvasive estimation of PAP.

Adolescent↗

[Local thrombolysis of renal artery embolism].

Thrombo-embolic occlusions of the renal arteries are usually a result of co-existing cardiac disease, in most cases cardiac arrhythmias or ischaemic heart disease. Similar findings have been observed in mesenteric infarction and embolism into the lower extremities. The duration of ischaemia determines the prognosis. Surgical intervention has been the mainstay of previous therapy. However, the application of local thrombolysis, which is an extension of the diagnostic catheter studies, provides an alternative form of treatment. As in the case of peripheral artery disease, the choice of treatment can only be made in consultation with the surgeon. This report presents experience with the use of local thrombolysis of renal artery emboli.

Aged↗

Q-T prolongation and torsades de pointes in a patient with subarachnoid hemorrhage.

An extreme Q-T prolongation in a patient with subarachnoid hemorrhage was observed. Multiple torsades de pointes occurred. Lidocaine, metoprolol, and atropine were not effective in controlling the arrhythmia, whereas shortening the Q-T interval by intravenous administration of orciprenaline or overdrive ventricular pacing was successful. The occurrence of T wave alternations was a sign of increased sympathetic activity.

Aged↗

Sudden cardiac death recorded during ambulatory electrocardiographic monitoring.

Two case reports of sudden cardiac death are detailed here. Holter monitoring plays an important role in documenting arrhythmias leading to sudden cardiac death. In addition, the importance of the Lown grading concept should not be underestimated. Our two case reports and a subsequent review of the literature demonstrate both points.

Aged↗

[Prognostic significance of the QT-interval following myocardial infarction].

The prognostic value of QT prolongation was evaluated in 109 patients with myocardial infarction. Patients who suffered from reinfarction during the first month or developed ventricular fibrillation and sudden death did not have longer QT intervals than patients without these complications. On the other hand, QT prolongation was of prognostic value in the prediction of late reinfarction. The reasons for varying results from different investigators are discussed.

Adult↗

Flecainide-induced aggravation of ventricular tachycardia.

Flecainide acetate is a new class I antiarrhythmic agent which slows atrial, A-V nodal and ventricular conduction velocity, and prolongs refractoriness of these structures (Borchard et al., 1982; Hodess et al., 1979). Recent studies with oral flecainide therapy suggested its high potential for suppression of ventricular tachycardia in humans (Anderson et al., 1981; Duff et al., 1981; Hodges et al., 1982). Its favorable pharmacokinetics with an average plasma half-time of about 20 hours allows in most patients twice daily dosing (Duff et al., 1981). Usually, the drug seemed to be well tolerated and side-effects, such as blurred vision, could be resolved with smaller but still effective doses (Duff et al., 1981). Actually, the ideal antiarrhythmic agent which represents a high degree of effectiveness, a low level of toxicity, a wide therapeutic range, and a prolonged antiarrhythmic action does not exist (Dreifus and Ogawa, 1977). In this report we describe a patient with flecainide-induced aggravation of ventricular tachycardia necessitating resuscitation because of severe hemodynamic deterioration.

Anti-Arrhythmia Agents↗

Electrophysiological studies on effects of AQ-A 39 in the isolated guinea pig heart and myocardial preparations.

An isolated perfused hearts as well as in papillary muscles and in Purkinje fibres, the influence of 5,6-dimethoxy-2(3[alpha-(3,4-dimethoxy)phenylethyl)-methylamino]propyl)phthalimidine hydrochloride (AQ-A 39) on the electrical activity was examined (concentration range of AQ-A 39 2.15--10.7 x 10-(5) mol/l). In the isolated heart AQ-A 39 (2.15 x 10(-5) mol/l) reduced the sinus frequency by about 50%. Higher concentrations (up to 10.7 x 10(-5) mol/l) exerted only little additional influence. Similar effects of AQ-A 39 were observed in Ba2+ induced pacemakers in the ventricular myocardium. In Purkinje fibres (K+e 2.7 x 10(-3) mol/l) AQ-A 39 (2.15 x 10(-5) mol/l) reduced the rate of spontaneous discharge to a considerable extent. In papillary muscles as well as in Purkinje fibres the terminal phase of repolarization of the action potential was markedly prolonged without a detectable influence on the resting potential or the maximal rate of rise (Vmax). In the Ba2+ treated depolarized myocardium Vmax was considerably reduced by AQ-A 39. The effects of AQ-A 39 are discussed in view of their ionic mechanisms as well as of the therapeutic application of the drug.

Action Potentials↗

Factors determining the susceptibility of the isolated guinea pig heart to ventricular fibrillation induced by sinusoidal alternating current at frequencies from 1 to 1000 Hz.

We determined the threshold for ventricular fibrillation by means of sinusoidal alternating current (AC) from 1 to 1000 Hz on isolated perfused guinea pig hearts. Current was applied via electrodes located in the aorta and at the apex of the heart. The duration of current flow was kept constant at 1 s. Electrical activity was recorded with epicardial electrodes attached to the ventricles. Additional experiments were performed in isolated papillary muscles with intracellular microelectrodes. The fibrillation threshold, expressed as peak-to-peak current strength, attains a minimum at about 30 Hz and rises by a factor of 5 at 1 Hz, and by a factor of 14 at 1000 Hz. In the frequency range from 30 to 1000 Hz the rise of the fibrillation threshold can be attributed to the increase of the threshold for stimulation due to the progressive shortening of the AC periods. Thus no change of the fibrillation threshold occurs if DC pulses of constant duration are used in the same range of frequencies. Below 30 Hz there is only a slight increase of the threshold for stimulation, which cannot entirely account for the rise of the threshold for fibrillation. A likely cause of the reduced susceptibility of the heart to fibrillation at the lower frequencies is the reduced number of extrasystoles preceding the onset of fibrillation, which results in a less pronounced state of inhomogeneous excitability.

Acoustics↗

Effects of changes in frequency on guinea pig ventricular action potential duration and on QT interval under different experimental conditions.

Isolated perfused guinea pig hearts (Langendorff preparation) were arrested by carbachol (0.1-0.2 mg/l) and electrically stimulated in the region of the av-conducting system. The QT interval was determined by means of extracellular electrodes at different driving frequencies. Separate experiments were performed on papillary muscles from the right ventricle to measure the duration of the transmembrane action potential under comparable conditions. At 35 degrees C (Ke+ 5.4 mmol/l) increasing the frequency of stimulation (range 12-120/min) caused the action potential duration (APD) to decrease to a greater extent than the QT interval. Stepwise rising of the external K+ concentration up to 16.2 mmol/l produced a nearly parallel shift to the APD-frequency relation to lower values. Again, the QT interval was less affected by increasing the external K+ concentration than the APD. Stepwise reduction of the temperature down to 20 degrees C prolonged the APD as well as the QT interval, the effects being more pronounced at lower than at higher stimulation frequencies. Under all examined experimental conditions, the APD proved to be markedly shorter than the QT interval even when the latter is diminished by the duration of QRS. The results suggest that no close relation exists between the APD and the QT interval. The observed divergencies may be due to functional differences among various parts of the ventricles.

Action Potentials↗

Influence of direct current on the electrical activity of the heart and on its susceptibility to ventricular fibrillation.

Isolated perfused guinea pig hearts (Langendorff preparation) were used to study the influence of direct current (DC) on the shape of the electrogram and to determine the thresholds for extrasystoles and for fibrillation. DC impulse durations ranged between 30 ms and 5 s. During DC flow through the heart, marked deformations of the electrogram occur mainly concerning the repolarization phase and increasing with growing current strength. At an intensity of twice the diastolic threshold for stimulation, constant DC induces extrasystoles, which are suggested to result from an enhancement of the intrinsic automatic activity by cathodal polarization. Compared with the diastolic threshold for stimulation, the threshold for fibrillation is higher by a factor of about 15. The curve relating the threshold for fibrillation to the impulse duration shows a marked decline between 30 ms and 60 ms, followed by a slight increase and adjustment to a constant level beyond about 80 ms. In the used setup, the threshold for fibrillation is independent on the reversal of polarity of the electrodes. Long-lasting DC pulses are able to induce fibrillation even if they are switched on in the absolute refractory period of a normal beat. Application of 50-Hz alternating current revealed a higher threshold for stimulation and a three times lower fibrillation threshold compared with the effects of DC in the same heart.

Animals↗

Effects of mexiletine on steady-state characteristics and recovery kinetics of V max and conduction velocity in guinea pig myocardium.

We studied the effect of the antiarrhythmic compound mexiletine on the maximal rate of rise (V max) on the action potential and on conduction velocity in isolated papillary muscles of guinea pigs. Action potentials and V max were measured by means of conventional microelectrodes. The conduction velocity was determined from extracellular recordings Mexiletine (concentrations, 4.6 x 10(-5) and 1.15 x 10(-4) mol/L) caused a depression of V max that depended on the condition examined. The h infinity curve relating V max of the action potential to the resting membrane potential was shifted along the voltage axis to more negative membrane potentials. Qualitatively equal effects were observed on the curve of membrane responsiveness relating V max to the membrane potential during the phase of repolarization of the preceding action potential. Eventually, marked prolongation of the recovery kinetics of V max by mexiletine, as well as frequency-dependent reduction of V max, could be demonstrated. The action of mexiletine on conduction velocity was very similar to its influence on V max. Thus, prolongation of the recovery kinetics was found of about the same magnitude as that measured in V max. Similarly, in experiments with K + -induced depolarizations, a dependence on the membrane potential of the action of mexiletine on the conduction velocity could be demonstrated. The results suggest that mexiletine may exert antiarrhythmic effects mainly in damaged cardiac cells exhibiting a moderately reduced resting potential.

Action Potentials↗