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W Doering

Publications and source records attributed to W Doering.

At least 19 recordsLinked to original sources
PubMed1995

Determinants of dual chamber pulse generators longevity.

The aim of this study was to investigate the effect of battery capacity, internal current drain, and stimulation energy on pulse generators longevity, and if battery impedance measurements can reliably predict pulse generators end-of-life. For this purpose, the records of 577 patients with a mean age of 65 +/- 14 years who had undergone implantation of two different dual chamber pulse generators (PG1: 409; PG2: 168) were retrospectively reviewed. Battery capacity were 2.3 Ah (PG1) and 3.0 Ah (PG2) while current drain at comparable nominal settings was 20 microA (PG1) and 30 microA (PG2) indicating a higher internal current drain of PG2. After a mean follow-up of 46 +/- 23 months, stimulation energy at reprogrammed output settings was significantly higher in PG1 as compared to PG2 (17.1 +/- 0.14) vs 15.5 +/- 0.24 J). Three PG1 (0.7%) and 12 PG2 (7.1%) (P < 0.01) had to be exchanged after a mean of 77.3 +/- 5.3 months (PG1) and 75 +/- 13.5 months (PG2) (P = NS) due to end-of-life being reached. The difference in battery impedances of PG1 and PG2 gained statistical significance 5 years after implantation (1.0 k omega vs 2.4 +/- 6.7 k omega) preceding the significant difference in PG survival after 6 years (98.7 +/- 1.3% vs 90.7 +/- 4.8%). These results indicate that internal current drain is the most important determinant of the pulse generators longevity and that battery impedance can reliably predict end-of-life. Therefore, the essential information about internal current drain should be available for each pacemaker, since it is required for adequate pulse generator selection. Diagnostic functions of dual chamber pulse generators should include measurements of battery impedance.

Adult↗
PubMed1994

[Ergospirometry in the evaluation of cardiovascular drugs].

In the evaluation of drugs intended to alleviate symptomatology and to improve exercise capacity in congestive heart failure, various pathophysiologic mechanisms including impairment of cardiac output, oxygenation of blood, muscle blood flow, and muscle metabolism have to be considered. In various forms of acute and chronic heart failure these mechanisms contribute more or less to impaired oxygen uptake. In acute forms of heart failure pulmonary congestion and its effects on airway resistance and lung capacity might be the predominating mechanisms of symptoms, while in chronic heart failure impedement of muscle blood flow and metabolic changes, comparable with deconditioning, are additional pathomechanisms. The increase in cardiac output and in muscle blood flow provided by some positive inotropic agents and by vasodilators after acute administration is often paralleled by a decrease in arteriovenous oxygen difference and does not lead to an improvement of oxygen uptake. However, chronic therapy with some vasodilators can lead to improvement in oxygen uptake, either due to training effects or due to flow dependent or direct effects on muscle metabolism. In pulmonary congestion a decrease of elevated filling pressures can acutely lead to some improvement of exercise capacity. Furthermore, chronic decrease in filling pressures by administration of diuretics, nitrates, ACE-inhibitors or dopaminergic drugs leads to long-term improvement in oxygen uptake. By comparing hemodynamic effects of acute and chronic drug therapy in CHF with their effects on exercise capacity, the chronic decrease of filling pressures seems to be the major hemodynamic variable leading to improvement of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiotonic Agents↗
PubMed1993

Experiences with ACE inhibitors early after acute myocardial infarction. Rationale and design of the German Multicenter Study on the Effects of Captopril on Cardiopulmonary Exercise parameters post myocardial infarction (ECCE).

Left ventricular damage by necrosis of myocardial tissue can lead to compromise of left ventricular function, to left ventricular volume increase and ultimately to development of heart failure. This sequence in the pathophysiology has been shown to be blunted by ACE inhibitors. Volume increase, however, can also be helpful in restoring stroke volume and ameliorate elevation of filling pressures. Furthermore, very early institution of ACE inhibition has failed to improve short-term mortality after myocardial infarction in one large trial. The aim of the ECCE trial therefore is, to investigate the early effects of the ACE inhibitor captopril on compromise of exercise capacity, thought to be a first measurable sign of developing heart failure. The ECCE trial is a randomized, seven-center investigation, studying the effects of ACE inhibition on oxygen uptake in a double blind, placebo controlled design in a group of 204 patients. Sample size was calculated on the basis of a pilot trial. The study design and first not unblinded data of 104 patients are presented. The population consists of predominantly male patients with mostly first myocardial infarction. They were admitted to hospital within five hours of onset of chest pain. End-diastolic volumes were normal, but ejection fraction was moderately compromised. ACE inhibition was started after the first day, but within 72 hours of onset of chest pain. After four and after twelve weeks, oxygen uptake was considerably below expected values and one third of the patients had severe compromise of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Impact of converting enzyme inhibition on progression of chronic heart failure: results of the Munich Mild Heart Failure Trial.

OBJECTIVE: Neurohormonal activation has major impact on the pathophysiology of congestive heart failure. The Munich Mild Heart Failure Trial was designed to test the hypothesis that interference with the renin-angiotensin system by angiotensin converting enzyme inhibition favourably influences the natural history of heart failure. DESIGN AND PATIENTS: 170 patients, median New York Heart Association (NYHA) class II, were randomised to double blind treatment with 25 mg captopril twice a day or placebo in addition to standard treatment for a median observation period of 2.7 years. MAIN OUTCOME MEASURES: Progression of heart failure to NYHA class IV on an optimally adjusted standard treatment, death due to progressive heart failure, and sudden death. RESULTS: Heart failure progressed to class IV in nine patients (10.8%) treated with captopril and in 23 patients (26.4%) treated with placebo (p = 0.01). The mean survival time until this end point was 223 days longer in the captopril group (Kaplan-Meier life table analysis; p = 0.02). Also, progressive deterioration to severe heart failure was a powerful predictor of total mortality and death from heart failure; 80% of deaths due to progressive heart failure occurred after this end point. There were fewer deaths caused by progressive heart failure in the captopril group than in the placebo group (4 v 11; p = 0.10) but similar numbers of sudden deaths (11 v 10). Progressive heart failure was the cause of death in 18.2% of all deaths in the captopril group and 50% in the placebo group. Total heart failure events (the end point on which power calculation was based) were also more common in the placebo group (19 v 32 events) but not significantly so. Total mortality was similar to both groups (22 of 83 v 22 of 87). CONCLUSIONS: Angiotensin converting enzyme inhibition in conjunction with standard therapy early in the course of congestive heart failure slowed the progress of heart failure and thus favourably altered the natural history of the disease.

Adolescent↗
PubMed1992

Mechanisms involved in cardiac enlargement and congestive heart failure development after acute myocardial infarction.

For 3 months, we followed up 40 patients with acute myocardial infarction, 20 were randomly assigned to treatment with captopril and 20 to placebo, to elucidate mechanisms inducing left ventricular volume enlargement and development of congestive heart failure. Echocardiographic follow-up could be obtained in 28 patients, 11 of whom showed more than a 10% increase in left ventricular systolic and/or diastolic volumes (captopril n = 3/15, placebo n = 8/13, p = 0.05). Volume increase was significantly associated with an impairment in exercise capacity (VO2 max in patients with vs. without volume enlargement 24.7 +/- 1.7 vs. 29.5 +/- 1.9 ml O2/kg/min; p < 0.05). Plasma renin activity, angiotensin II and catecholamines were normal in the acute and chronic postinfarction phase in patients on placebo as well as in patients 12-24 h after captopril intake. Plasma atrial natriuretic peptide concentration (ANP) was increased immediately after myocardial infarction, but ANP levels almost normalized in patients with captopril treatment, while they continued to be elevated in patients on placebo. The only technical parameter able to predict left ventricular volume increases was the sphericity index (28.7 vs. 35.7; p = 0.07). We concluded that morphologic deformation and filling pressures as estimated from elevated ANP levels are major factors promoting remodelling following myocardial infarction. ACE inhibitors might exert their favorable effect predominantly by reducing filling pressure.

Atrial Natriuretic Factor↗
PubMed1991

Influence of severity of heart failure on the efficacy of angiotensin-converting enzyme inhibition.

Angiotensin-converting enzyme (ACE) inhibition slowed the progression of congestive heart failure (CHF) in 170 patients who were randomly assigned to either captopril or placebo in the Munich Mild Heart Failure Trial. The two major end points were progression from New York Heart Association (NYHA) functional classes I, II, or III to class IV, despite optimal, adjusted standard therapy, and death due to CHF. The relative risk for progressive CHF with captopril therapy was 0.34 (95% confidence interval = 0.17-0.68; p = 0.01). A total of 52 prerandomization variables were tested to determine their contribution to disease progression. Logistic regression analysis revealed 5 independent risk factors for progressive CHF: NYHA class, left ventricular end-systolic diameter, need for diuretic, age, and cardiothoracic ratio. The presence of greater than 2 of these risk factors increased the odds ratio for progression to 8.13 (p less than 0.001) compared with the presence of 0-2 risk factors. However, the effectiveness of captopril in preventing progression was higher within the subgroup of patients who had less severe CHF: the odds ratio was 0.12 (95% confidence interval = 0.03-0.45; p less than 0.01) for patients in NYHA class I or II on captopril and was 0.83 for those in class III. We conclude that the severity of CHF, as represented by the above-defined risk factors, is directly related to the likelihood for the development of progressive heart failure. However, the less severe the heart failure, the more effective the treatment with captopril will be in preventing disease progression. Thus, ACE inhibition has considerable potential for improving the prognosis of patients with mild heart failure.

Age Factors↗
PubMed1991

[Prognosis of mild chronic heart failure: effects of the ACE inhibitor captopril].

UNLABELLED: The Munich Mild Heart Failure Trial (MHFT) investigated the influences of ACE-inhibition on progression of congestive heart failure (CHF). Major end points were progression of CHF from New York Heart Association (NYHA) functional classes I to III to NYHA functional class IV despite optimal adjusted standard therapy and death due to congestive heart failure, i.e. death due to pump failure or sudden death. 170 patients were randomly assigned to treatment with either captopril (n = 83) 25 mg b.i.d. or placebo in addition to standard therapy for a median observation period of 2.7 years. The major result of this trial was the decrease in the relative risk for progressive heart failure by captopril therapy to 34% (95% confidence interval 17 to 68%; p = 0.01). Though total mortality was not reduced, death due to pump failure was found considerably less often on captopril than on placebo (18.2 vs 50% of total deaths in each group). In addition this report describes influences of captopril therapy on left ventricular size and function, heart size on X-ray, influences on symptomatology, electrolytes, ventricular arrhythmias, on concomitant therapy as well as effects in various subgroups. The major finding of the trial--the influence on progression of CHF--was independent of the underlying cardiac disease and was consistent in subgroups with different etiology of heart failure. Captopril blunted the increase in norepinephrine levels usually seen with increasing severity of congestive heart failure. There was a significant increase in serum sodium and potassium levels in the captopril treated group. Left ventricular size and function were well preserved in the patients still on randomized therapy after two years. No effects of therapy on ventricular ectopic activity were found in a subgroup of 93 patients that had had Holter monitoring. IN CONCLUSION: Captopril has marked effects on progression of disease and reduces the likelihood of progressive heart failure in patients with mild symptoms. Several indices of unfavourable prognosis are either improved (sodium, norepinephrine, angiotensin II) or stabilized (left ventricular function). Thus ACE-inhibitors are to be considered for all patients requiring medical therapy for congestive heart failure.

Captopril↗
PubMed1990

[The prognostic significance of lymphocyte subpopulations and macrophages in peripheral blood and in bronchoalveolar lavage in AIDS patients with suspected Pneumocystis carinii pneumonia].

In 36 HIV seropositive patients with the clinical manifestation of AIDS and a suspected Pneumocystis carinii infection, lymphocyte subpopulations were analyzed in the peripheral blood (PBL) and compared with the results of the bronchoalveolar lavage (BAL). Of those 36 patients, 29 showed a highly abnormal CD4/CD8 ratio in both the PBL and the BAL. The clinical course of these 29 patients was unpredictable. In seven patients, however, the CD4/CD8 ratio in the BAL was normal or only slightly altered, despite a highly abnormal CD4/CD8 ratio in the PBL. Five of these seven patients improved greatly during the clinical course. The positive outcome of the clinical course was even more strongly correlated with the number of macrophages in the BAL. Twelve of the 36 patients showed normal or only slightly changed numbers of macrophages in the BAL. Eleven of these twelve patients (92%) improved rapidly during antibiotic therapy, while the clinical course was unpredictable in patients with markedly reduced macrophage counts in the BAL.

Acquired Immunodeficiency Syndrome↗
PubMed1990

Persistent atrioventricular block in Lyme borreliosis.

Cardiac manifestations are reported in 0.3%-4.0% of European patients with Borrelia burgdorferi (B.b.) infection. Usually symptoms disappear within 6 weeks. We report a case with persistent impairment of atrioventricular (AV) conduction. Diagnosis was confirmed by demonstration of IgM antibodies and increase of IgG antibody titers against B.b. in serum, by isolation of the spirochete from skin biopsy material and by the typical clinical combination of erythema migrans, Bannwarth syndrome (meningoradiculitis), and complete heart block. Despite immediate antibiotic therapy with ceftriaxone, first degree AV block and second degree block Wenckebach with atrial pacing at 100 beats/minute persisted for 2 years. We conclude, that Lyme carditis can cause long-standing or irreversible AV conduction defects despite adequate and early antimicrobial therapy.

Adult↗
PubMed1990

[Progressive left ventricular dilatation following anterior myocardial infarct as a determinant for the development of heart failure].

35 consecutive patients were studied prospectively with respect to echocardiographic left ventricular size after anterior myocardial infarction. In 25 patients sufficient follow-up was possible. Another 57 patients and volunteers were examined to prove accuracy in comparison to angiocardiography and nuclear magnetic resonance imaging and reproducibility as well as to define normal values. While two-thirds of all patients did not develop left ventricular dilation, one-third showed marked dilation with left ventricular size being 41% above mean normal value. All patients who subsequently developed congestive heart failure or died were in this group. Two-thirds showed no left ventricular dilation and had an uneventful follow-up. Mean left ventricular dilation for all infarcts was 22% within 4 weeks and 26% within 6.3 months, but some patients showed marked left ventricular dilation beyond 4 weeks. We conclude that serial echocardiography is very useful for stratification of risk for CHF after myocardial infarction, and left ventricular dilation is a major risk factor for CHF.

Adult↗
PubMed1988

Left ventricular relaxation and filling pattern in diabetic heart muscle disease: an echocardiographic study.

In order to study left ventricular function digitized M-mode-echocardiograms were analyzed. 34 patients with insulin-dependent diabetes mellitus (mean age 37.8 years, mean diabetes history 21.5 years) were compared with 35 healthy individuals (mean age 40.9 years). Only patients with negative exercise-ECG, normal 2-D-echocardiogram and normal systemic arterial blood pressure were enclosed. In diabetics the time-constant Te of free wall endocardial retraction was significantly prolonged (76.8 +/- 21.2 ms versus 64.0 +/- 7.9 ms in normals, p less than 0.005), the dimension change during early diastole (dD DS-ERF) was significantly reduced (54.5 +/- 13.1% versus 69.8 +/- 9% in normals, p less than 0.001) and the dimension change during atrial contraction phase (dD ACP) was significantly enlarged (23.4 +/- 14.4% versus 14.3 +/- 6.4% in normals, p less than 0.001). These data suggest that impaired left ventricular diastolic function can be found in patients with long standing insulin-dependent diabetes mellitus.

Adolescent↗
PubMed1988

Effects of enzymatic blood defibrination in subcortical arteriosclerotic encephalopathy.

Plasma hyperviscosity is a striking abnormality in patients suffering from subcortical arteriosclerotic encephalopathy (SAE) and is thought to perpetuate the chronic ischaemic demyelinating process of the periventricular white matter. Ancrod, a defibrinating enzyme, was given to 10 patients with SAE in an attempt to reduce plasma fibrinogen, which would thus normalise hyperviscosity. This was paralleled by a significant improvement of the initially abnormal retinal arteriovenous passage time, as well as a significant augmentation of the CO2-induced cerebral vasomotor response. This did not lead, however, to any clinical improvement with respect to performance of neuropsychological tests, recurrences of strokes during a 6 month observation period or improvement of various audiological parameters. The findings indicate that hyperviscosity in patients with SAE is merely an epiphenomenon. A potentially reversible, chronic penumbral state of the brain tissue apparently does not exist in SAE.

Aged↗
PubMed1987

Pharmacokinetic interaction study with ramipril and digoxin in healthy volunteers.

Coadministration of captopril has been shown to increase serum digoxin concentration. The effects of ramipril, a new angiotensin converting enzyme inhibitor, on serum digoxin concentration after multiple dosing were studied in 12 healthy volunteers. All subjects were receiving steady-state digoxin medication (0.5 mg daily), and ramipril (5 mg daily) was coadministered for 14 days. Serum digoxin concentration was measured repeatedly before, during and up to 1 week after ramipril coadministration at 8 a.m. (trough values) and on selected trial days at 11 a.m., 3 hours after the morning medication. Simultaneously, blood levels of ramipril and its active metabolite diacid were determined. Volunteers were followed closely for side effects and for changes in blood pressure, heart rate and electrocardiogram. Safety pharmacology included serial determination of sodium, potassium, serum glutamic oxaloacetic transaminase, creatinine and a full blood count. Mean serum digoxin concentration was not significantly influenced by ramipril coadministration with trough levels of 0.90 +/- 0.24 before, 0.93 +/- 0.38 during and 0.82 +/- 0.33 ng/ml after ramipril medication. The increase in serum digoxin concentration 3 hours after the morning dose was also not significantly affected by ramipril. Serum levels of ramipril and its diacid showed a wide range of variation. Mean serum potassium increased by 0.3 mmol/liter during ramipril coadministration with development of symptomless hyperkalemia (6.0 mmol/liter) in 1 subject. The only other side effect possibly related to ramipril was a dry cough in 1 subject. Both drugs were well tolerated. Ramipril showed no significant influence on serum digoxin levels in healthy volunteers.

Adult↗
PubMed1985

Influence of quinidine on the intestinal secretion of digoxin and digitoxin in guinea pigs.

The secretion of digoxin and digitoxin into in situ perfused jejunal and colonic segments of normal or quinidine treated guinea pigs was studied. Quinidine was administered intravenously by constant rate infusion resulting in a quinidine plasma concentration of about 6 micrograms/ml. After 2 h digoxin or digitoxin was injected i.v. (10 micrograms/kg). The quinidine treatment enhanced the plasma concentration of [3H]digoxin to about 140% as compared to controls, whereas the [3H]digitoxin concentration was not influenced by the quinidine infusion. Both, digoxin and digitoxin were secreted against a concentration gradient into the intestinal lumen. During the experimental period of 180 min controls secreted 0.24% of the administered digoxin dose per cm of jejunal and 0.13% per cm of colonic segment. Quinidine treatment resulted in a decrease of the jejunal digoxin secretion to about 80% of the control values. In both, jejunum and colon the concentration ratio between lumen and plasma (L/P) was diminished by quinidine to 50% as compared with the controls. The amount of [3H]digitoxin secreted into the intestinal segments was decreased by quinidine from 0.19% of the dose/cm to 0.13% in the jejunal and from 0.17% to 0.12% in the colonic segments, respectively. The decrease of the L/P ratio for [3H]digitoxin was more pronounced in the colon (58%) than in the jejunum (77% of the control values). As compared with controls the content of [3H]digoxin in the jejunal as well as colonic tissue was decreased by quinidine to 60% or 73%, respectively. On the other hand quinidine increased the tissue content of [3H]digitoxin in jejunum (+56%) and colon (+88%). In conclusion quinidine inhibits the intestinal secretion of both, digoxin and digitoxin, possibly by different mechanisms.

Animals↗
PubMed1983

Effect of coadministration of verapamil and quinidine on serum digoxin concentration.

Both quinidine and verapamil are known to increase the serum digoxin concentration (SDC), and other calcium channel blockers may have a similar effect. Since an increasing number of patients is likely to be treated concurrently with digoxin, quinidine and a calcium channel blocker, a study was done to show whether coadministered quinidine and verapamil would cooperate to elevate the SDC. Nine healthy volunteers on basic digoxin treatment (Leanoxin 0.125 mg t.i.d.) were treated with placebo, verapamil 80 mg t.i.d. and the combination (verapamil 80 mg plus quinidine base 160 mg t.i.d.), for 2 weeks in a randomized sequence. Drug concentration and various cardiovascular parameters were measured each week and/or at the end of each treatment period. Steady state concentrations were always obtained within 1 week and drug levels at the end of the first and second weeks of treatment were almost identical. The plasma verapamil concentration (PVC) was 25.8 +/- 9.9 ng/ml during coadministration of verapamil and digoxin, and 15.7 +/- 6.9 ng/ml during combined verapamil-quinidine coadministration, when the serum quinidine concentration (SQC) was 1.26 +/- 0.50 micrograms/ml. Compared to placebo SDC rose by 53% from 0.62 +/- 0.16 to 0.95 +/- 0.29 ng/ml (p less than 0.001) during verapamil treatment and further to 1.58 +/- 0.38 ng/ml (155% rise; p less than 0.001) during combined verapamil-quinidine coadministration. Thus each drug maintained its own effect on SDC in the presence of the other, and their actions became combined in increasing the SDC.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

Interaction between digoxin and calcium antagonists and antiarrhythmic drugs.

The influence of several calcium antagonists and antiarrhythmic drugs on digoxin kinetics and actions were investigated in 36 healthy men during digoxin steady state (0.375 mg/day). The subjects were randomly assigned to three subgroups and each group received placebo (control) and two of the following regimens (doses three times a day) in a randomized sequence for 2 wk each: verapamil (80 mg) and nifedipine (10 mg), verapamil (120 mg) and gallopamil (50 mg), or propafenone (150 mg) and quinidine (250 mg). Plasma digoxin concentration (PDC) rose during the cotreatments in the sequence: gallopamil (+16%) less than propafenone (+37%) less than nifedipine (+45%) less than verapamil (almost independent of dose, +69%) less than quinidine (+118%). These increases in PDC correlated closely to decreases in renal digoxin clearances. Renal creatinine clearance was virtually unaffected. The rise of PDC resulted in increased glycoside effects, as measured by the shortening of systolic time intervals and flattening of T wave. There was a linear correlation between PDC and changes in mean corrected electromechanical systole and T wave flattening. We conclude that, in addition to quinidine, other antiarrhythmic drugs and various calcium antagonists interact kinetically with digoxin and that the increasing PDCs are cardioactive.

Adult↗