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Biomedical subjects

W W Klein

Publications and source records attributed to W W Klein.

At least 19 recordsLinked to original sources
PubMed2002

Rescue percutaneous transluminal coronary angioplasty in a patient with a single coronary artery arising from the right Sinus Valsalvae: previously unreported scenario and review of literature.

This is the first description of treatment with coronary stenting of a patient with a single coronary artery originating from the right Sinus Valsalvae and suffering from acute inferior myocardial infarction. Angiography showed the following: the right coronary artery (RCA) had a normal course, whilst the left anterior descending (LAD) as well as the left circumflex (LCX) branches both originated separately from the proximal RCA, which served as a common mixed trunk. The LAD crossed to the left in front of the right ventricular outflow tract, whilst the LCX, taking a retroaortic course to the atrioventricular groove, had a distal occlusion. According to an anatomically based classification considering all imaginable variations, this configuration corresponds to a II-D-1 pattern, which previously has been described only in a single postmortem case. After the LCX was reopened with a guide wire, a coronary stent was successfully inserted, resulting in TIMI-3 flow. Recovery was uneventful.

Angioplasty, Balloon, Coronary↗
PubMed2001

ACC/AHA/ESC Guidelines for the Management of Patients With Atrial Fibrillation: Executive Summary A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation) Developed in Collaboration With the North American Society of Pacing and Electrophysiology.

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Aged↗
PubMed2001

ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation: executive summary. A Report of the American College of Cardiology/ American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to Develop Guidelines for the Management of Patients With Atrial Fibrillation): developed in Collaboration With the North American Society of Pacing and Electrophysiology.

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Algorithms↗
PubMed2001

ACC/AHA/ESC guidelines for the management of patients with atrial fibrillation. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines and Policy Conferences (Committee to develop guidelines for the management of patients with atrial fibrillation) developed in collaboration with the North American Society of Pacing and Electrophysiology.

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Atrial Fibrillation↗
PubMed1999

Natriuretic peptides in patients with diastolic dysfunction due to idiopathic dilated cardiomyopathy.

AIMS: The degree of systolic dysfunction does not always correlate with functional impairment in patients with congestive heart failure. In contrast, diastolic dysfunction correlates well with functional impairment. In heart failure, both elevation of N-terminal proatrial natriuretic peptide and B-type natriuretic peptide are markers of a poor prognosis. METHODS: We investigated 32 patients (26 male, 6 female; mean age 55+/-2 years) with dilated cardiomyopathy and sinus rhythm. M-mode echocardiography and 2D-echocardiography were carried out in each patient. Pulsed-wave Doppler inflow signals were obtained and the following parameters were measured: maximal E wave and maximal A wave velocity, E/A ratio, E wave deceleration time, A wave deceleration time. Immediately after echocardiography blood samples were collected from patients in the supine position. N-terminal proANP and brain natriuretic peptide were measured using a radioimmuno assay. RESULTS: The left ventricular ejection fraction was 34+/-1%, the left ventricular end-diastolic diameter on M-mode echocardiography was 68+/-1 mm, while left atrial diameter was 45+/-1 mm. Univariate analysis revealed a significant correlation between both left atrial diameter and ejection fraction and N-terminal proANP and brain natriuretic peptide. All transmitral Doppler parameters showed a significant correlation with N-terminal proANP and brain natriuretic peptide. On forward stepwise regression analysis, left atrial diameter and ejection fraction were able to predict both N-terminal proANP and brain natriuretic peptide. However, of the diastolic parameters only the E/A ratio remained significant. Mildly symptomatic patients differed significantly from severely symptomatic patients in all Doppler parameters. Mildly symptomatic patients had significantly lower levels of N-terminal proANP (0.571+/-0.079 vs 2.282+/-0.340 nmol. l(-1);P<0.001) and brain natriuretic peptide (51+/-14.8 vs 474.2+/- 86.8 pg. ml(-1);P<0. 001). CONCLUSION: There is a close relationship between natriuretic peptides and diastolic Doppler parameters of left ventricular filling in patients with dilated cardiomyopathy. There is also a significant difference between patients with mild and severe functional impairment regarding both natriuretic peptides and transmitral Doppler parameters.

Atrial Natriuretic Factor↗
PubMed1990

Effects of benazepril and metoprolol OROS alone and in combination on myocardial ischemia in patients with chronic stable angina.

The efficacy of benazepril, metoprolol OROS and their combination was evaluated in 29 patients (42 to 74 years of age) with chronic stable angina and documented coronary artery disease in a placebo-controlled, double-blind, crossover trial using serial quantitated exercise testing and ambulatory electrocardiographic (ECG) monitoring. The mean (+/- SEM) exercise time was 8.5 +/- 0.7 min with placebo, 8.3 +/- 0.6 min (95% confidence interval [CI]-1.06 to 0.54) with benazepril, 9.4 +/- 0.5 min (95% CI -0.32 to 2.14) with metoprolol OROS and 9.6 +/- 0.5 min (95% CI -0.25 to 2.47) with the combination of benazepril and metoprolol OROS. The mean exercise time to the development of 1 mm ST segment depression was prolonged from 6.0 +/- 0.6 min with placebo to 6.3 +/- 0.6 min (95% CI -0.93 to 1.45) with benazepril, 7.9 +/- 0.5 min (95% CI 0.83 to 3.0) with metoprolol OROS and 8.1 +/- 0.6 min (95% CI 0.88 to 3.29) with the combination of benazepril and metoprolol OROS. Benazepril did not alter the rest or maximal heart rate, whereas metoprolol OROS alone and in combination significantly lowered the heart rate at rest and during maximal exercise. Systolic blood pressure at rest was nonsignificantly reduced, whereas diastolic blood pressure was lowered significantly by all treatments in comparison with placebo. At maximal exercise, only metoprolol OROS, whether given alone or in combination with benazepril, was able to blunt significantly systolic blood pressure and rate-pressure product.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Antihypertensive therapy and coronary prevention.

Antihypertensive therapy reduces cardiovascular risk in patients with malignant hypertension, but has not yet been shown to reduce risk in patients with mild to moderate hypertension. The lack of significant coronary prevention in the latter group, in large-scale trials, may have resulted from methodologic problems, statistical limitations, the adverse effects of antihypertensive medications, or failure to recognize the prognostic importance of concomitant regression of left ventricular hypertrophy. To date, primary prevention studies have focused on the use of beta-blockers and diuretics, both of which may have adverse metabolic effects and neither of which is capable of modifying left ventricular hypertrophy. Future research should be directed toward evaluating coronary prevention in patients with nonmalignant hypertension who have been treated with newer agents, such as calcium channel blockers and angiotensin-converting enzyme inhibitors, each of which has been shown to regress left ventricular hypertrophy and not to have adverse metabolic effects.

Antihypertensive Agents↗
PubMed1986

Cross-over comparison between captopril and nifedipine.

In a cross-over study in 26 patients with mild to moderate essential hypertension The antihypertensive efficacy of captopril 25 mg b.i.d., nifedipine 20 mg b.i.d. and the combination both drugs in non-responders to monotherapy was compared. Of 26 captropril-treated patients 7 were non-responders and needed the addition of nifedipine; of 26 nifedipine-treated patients 3 needed additional captopril. Seven out of 26 patients treated with captopril, 22/26 patients given nifedipine and 9/10 patients receiving the combination reported side effects. In 3 nifedipine patients, 1 captopril patient and 1 patient on both drugs, treatment had to be stopped because of side effects. Captopril and nifedipine in these doses are about equally effective both after acute and chronic administration. The response-rate is somewhat higher with nifedipine, but the side effects are significantly less with captopril. There was no significant additive effect with the combination of the two drugs.

Captopril↗
PubMed1984

Treatment of hypertension with calcium channel blockers: European data.

In hypertensive emergencies, sublingual nifedipine (10 to 30 mg) is the treatment of choice. Nifedipine, however, may lead to reflex activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system as well as fluid retention when used as a monotherapy for a longer period of time. In chronic arterial hypertension, verapamil, and especially diltiazem seem to be superior to nifedipine. Verapamil (360 to 480 mg a day) and diltiazem (180 to 270 mg a day) produce a consistent antihypertensive effect throughout a 24-hour period. During dynamic or isometric exercise, their antihypertensive potency is equivalent to that of beta blockers. Overall response rate in patients with mild to moderate hypertension is 80 percent with monotherapy. In refractory hypertension, combination with thiazide, reserpine, or clonidine may be useful. Calcium blockers are preferred in older patients with chronic arterial hypertension, and in patients with low renin hypertension, coronary heart disease, peripheral vascular disease, or obstructive airways disease.

Age Factors↗
PubMed1980

Cardiovascular effects of mianserin--a comparative study with amitriptyline and a placebo in healthy subjects.

The cardiovascular effects of a tricyclic (amitriptyline) and a tetracyclic (mianserin) antidepressant were compared with those of a placebo in a double-blind randomized group-comparative trial stratified for sex in 18 healthy volunteers. The dose of the test preparations was gradually increased to therapeutic level. Duration of treatment was 8 days. Neither test drug affected objective physical condition, intraocular pressure, blood variables or urinalysis, and the effect on blood pressure was found to be negligible. No impressive differences of untoward cardiac effects between the test preparations could be demonstrated. However, the prolongation of the pre-ejection period in amitriptyline-treated males, indicating a negative effect on myocardial contractility, and the reduction of the left ventricular end-systolic volume by mianserin, probably through increasing the ejection fraction, are observations of possible clinical relevance. They lend further support to the assumption that therapeutic doses of tricyclic antidepressants may produce untoward cardiac effects whereas the tetracyclic mianserin seems devoid of such unwanted properties.

Adolescent↗
PubMed1979

[Exercise tolerance of patients with artificial cardiac pacemakers (author's transl)].

In order to determine their exercise tolerance, 20 patients with artificial ventricular demand pacemakers below the age of seventy were studied by bicycle ergometry. Only 30% of the patients showed a normal exercise tolerance according to the criteria by Kaltenbach, while 70% stopped the test prematurely because of leg fatigue, dyspnoe or chest pain. In terms of their exercise tolerance, there was no difference between patients who developed normal sinus rhythm or rapid atrial fibrillation during the exercise and those who remained at the fixed pacemaker rate throughout the test. It is concluded, therefore, that the exercise tolerance of pacemaker-patients is not only limited by the fixed heart rate but mainly by the underlying heart disease (coronary heart disease, cardiomyopathy, hypertensive heart disease etc.) and the general physical condition of the patients. In an age-matched control group of 20 patients 50% showed a normal exercise tolerance and the duration of exercise in this group was only slightly longer (21%) than in the pacemaker-group.

Aged↗
PubMed1978

[Preliminary hemodynamic studies on the activity of meproscillarin (author's transl)].

In 10 patients with arterial hypertension and left heart failure the hemodynamic effect of 14-hydroxy-3-beta-[4-O-methyl-alpha-L-rhamnopyranosyl)oxy]-14beta-bufa-4,20,22-trienolide (Ky 18, meproscillarin, Clift) was compared with placebo in a double-blind study. 15 min after oral administration of meproscillarin there was an increase of cardiac output and stroke volume by up to 25%. Heart rate, arterial blood pressure and left ventricular filling pressure remained unchanged.

Aged↗
PubMed1976

[Hemodynamic long-term effects of a beta-receptor blockader (Pindolol) in primary essential hypertension].

1. Pindolol lowers blood pressure both, immediately after administration by a reduction of cardiac output and heart rate and after long-term administration by reducing peripheral resistance. Cardiac index, initially decreased, reached the control value after 8 weeks of treatment. 2. The persistent reduction in heart rate and increase of the cardiac index during exercise after prolonged treatment together with the increase of right and left heart filling pressures seems to be due to augmentation of the Starling mechanism. The increase of the stroke volume at rest and during exercise diminished the blood-pressure lowering effect of the drug. 4. The exercise-induced increase of noradrenalin was abolished by acute administration of pindolol. After long-term treatment, however, we found a consistent and significant elevation of the plasma-catecholamines. This may reflect the development of heart failure [1], a tyramin- or cocain-like action of pindolol [2] or an indirect sympathicomimetic effect of this drug at low doses (10--15 mg/day orally ) [3]. 5. The elevation of plasma-noradrenalin reflects increased sympathetic tone and may be responsible for the increase in stroke volume and plasma renin activity observed by several authors. 6. Since there was no evidence for a hemodynamic mode of action, the lowering of blood rpessure by pindolol may be a central effect.

Blood Pressure↗