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Biomedical subjects

K Kochsiek

Publications and source records attributed to K Kochsiek.

At least 73 records · Page 4Linked to original sources
PubMed1990

Early remodelling of the left ventricle in patients with myocardial infarction.

Sequential alterations of left ventricular volumes and haemodynamics were studied in 29 patients between 4 days and 4 weeks after myocardial infarction. Left ventricular volume was determined by single photon emission computerized tomography (SPECT), infarct size by creatine kinase (CK) analysis, angiography and thallium201 SPECT. Left ventricular volume index (ml m-2) decreased in patients with small infarcts (74.5 +/- 4.9 vs 62.5 +/- 3.0, P less than 0.005), but increased significantly in patients with moderate (74.6 +/- 4.7 vs 83.6 +/- 5.0, P less than 0.0001) and large (71.7 +/- 4.8 vs 90.2 +/- 6.5, P less than 0.0001) infarctions between 4 days and 4 weeks after acute myocardial infarction. The latter groups contained almost two-thirds of our patients. This dilation occurred without significant changes in filling pressures (Swan-Ganz catheter) and resulted in significant augmentation and finally, normalization of stroke volume at 4 weeks (33.2 +/- 3.3 vs 42.6 +/- 2.9), despite persistently depressed ejection fraction (conventional radionuclide ventriculography). It is concluded that left ventricular dilatation post-myocardial infarction is structural (unchanged filling pressure) and compensatory (increased stroke volume) during the interval observed in this study.

Adult↗
PubMed1990

Comparative analysis of the action of class I antiarrhythmic drugs (lidocaine, quinidine, and prajmaline) in rabbit atrial and ventricular myocardium.

Effects of three class I antiarrhythmic drugs (quinidine, lidocaine, and prajmaline) on transmembrane resting (RMP) and action potentials (AP) of isolated rabbit atrial and ventricular myocardium were studied at different stimulation rates. The frequency-dependent depression of the maximal upstroke velocity (Vmax) of the AP (sodium channel block) was analyzed according to the "guarded receptor" hypothesis. The resting block (Vmax depression after a resting period) induced by prajmaline (10(-6) M), quinidine (2.2 x 10(-5) M), and lidocaine (4.3 x 10(-5) M) was more expressed in the atrium (44, 28, and 19%, respectively) than in the ventricle (32, 9, and 0%, respectively). There were also significant (p less than 0.05) atrioventricular differences in the frequency-dependent extra block (Vmax reduction on stimulation at 3.3 Hz) for quinidine (39 vs. 26%) and lidocaine (4 vs. 25%). From the analysis, according to the guarded receptor hypothesis, it follows that the three compounds bind preferentially to inactivated sodium channels with about the same affinity to the atrium and ventricle, except for quinidine which shows a significantly smaller dissociation constant in the atrium (5 x 10(-6) M vs. 2.7 x 10(-5) M; p less than 0.001). We conclude that the atrioventricular differences in the resting block are mainly due to atrioventricular differences in the RMP, whereas the differences in the frequency-dependent extra block are based on the shorter atrial AP duration (lidocaine) or are due to higher affinity to atrial sodium channels (quinidine).

Action Potentials↗
PubMed1990

Effects of endothelin-1 in isolated perfused rat heart.

We examined the effects of the vasoconstrictor peptide endothelin-1 in the isolated heart and defined interactions of endothelin-1 with other hormone systems. Isolated isovolumic rat hearts were perfused with Krebs-Henseleit buffer at constant pressure. First, the effect of a single bolus of endothelin-1 (4-400 pmol) was followed for 90 min. The effect of high dosages (40 and 400 pmol) of endothelin-1 on coronary flow was biphasic, with an early vasodilator and a late vasoconstrictor component that was irreversible. Second, cumulative dose-response curves were obtained for endothelin-1 boluses of 0.04-400 pmol. Coronary flow declined with increasing dosages and was almost abolished at 400 pmol. Neither alpha- nor beta-blocking agents (phentolamine and propranolol) nor the Ca2(+)-channel blocker nifedipine altered the effects of endothelin-1, but prostaglandin synthesis inhibition by indomethacin significantly augmented vasoconstriction by endothelin-1. Angiotensin-converting enzyme (ACE) inhibition by captopril antagonized endothelin-1-dependent vasoconstriction to a small extent at 400 pmol. Coronary constriction due to endothelin-1 could not be reversed by nitroglycerin. We conclude that in isolated rat heart endothelin-1 causes marked and long-lasting coronary constriction. The effect is not influenced by sympathetic and Ca2(+)-channel blockade, is enhanced by prostaglandin synthesis inhibition, and is reduced by ACE inhibition.

Adrenergic alpha-Antagonists↗
PubMed1990

Effects of endothelin-1 in the isolated heart under ischemic and cardioplegic conditions.

We examined the effects of the vasoconstrictor peptide endothelin-1 in isolated hearts under ischemic and cardioplegic conditions. Isolated isovolumic rat hearts were perfused with Krebs-Henseleit buffer at constant pressure. Cumulative dose-response curves were obtained for endothelin-1 boluses of 0.04-400 pmol in four groups of hearts. Coronary flow decreased with increasing dosages and was almost abolished at 400 pmol in control hearts perfused at a constant pressure of 100 mm Hg. In hearts made ischemic by reducing coronary perfusion pressure to 35 mm Hg, thus reducing coronary flow by 76%, the constrictor effect of endothelin-1 was well preserved. The endothelin-1 dose-response curve was unaltered when hearts were perfused with buffer containing 30 mM KCl to abolish mechanical activity without reducing extracellular Ca2+ concentration. A fourth group of hearts was perfused with Ca2(+)-free buffer, thus eliminating the source of extracellular Ca2+ as well as mechanical activity. In this group, the constrictor response to endothelin-1 was largely, but not completely, abolished, with a maximal constrictor effect of only 19% as opposed to 87% in control hearts. We conclude that in isolated rat heart endothelin-1 is a potent coronary constrictor under ischemic perfusion conditions and that absence of mechanical activity does not affect the action of endothelin-1, for which the presence of extracellular Ca2+ is essential. The small residual constrictor response with Ca2(+)-free perfusion is probably due to release of Ca2+ from intracellular stores.

Animals↗
PubMed1990

The six-minute walk--an adequate exercise test for pacemaker patients?

In many pacemaker patients bicycle and treadmill ergometry are not practicable. As an alternative, we performed a 6-minute walk on a 20-m corridor in 97 pacemaker patients, who were asked to walk as far as possible determining their speed by themselves. Results were compared with those of bicycle ergometry in 42 of these patients and with treadmill exercise of a group of 92 other pacemaker patients. In the 6-minute walk, performance and maximal heart rate were slightly lower (49 +/- 18 W; 96 +/- 23 beats/min) than in bicycle (57 +/- 16 W; 110 +/- 26 beats/min) and treadmill ergometry (50 +/- 37 W; 102 +/- 35 beats/min). A good correlation was found between walking and bicycling (r = 0.74) and in subgroups of patients with different pacemaker indications. All patients preferred the walk to bicycle ergometry considering it to be more related to daily physical activity. In conclusion, a 6-minute walk is a simple and physiological exercise test for nearly all pacemaker patients with good correlation to other types of exercise. It seems to be preferable to other tests because of its better acceptance and practicability.

Aged↗
PubMed1990

Symptoms, cardiovascular risk profile and spontaneous ECG in paced patients: a five-year follow-up study.

UNLABELLED: Only few data are available about the course of symptoms, cardiac diseases, and spontaneous rhythm in pacemaker patients. Therefore, we followed the course of 308 paced patients (age 72 +/- 11 years) with a mean implantation time of 63 +/- 45 months. RESULTS: The symptom triad of syncope, dizziness, and dyspnea improved remarkably in 93% of patients. Thirty-nine percent suffered from coronary heart disease. The risk factors of hypertension (47%), nicotine (37%), and diabetes mellitus (25%) were found significantly more often than in a normal population with the same age and sex profile. In VVI paced patients with sick sinus syndrome (SSS, n = 67) atrial fibrillation (AF) occurred significantly more often (42%) than in patients with AV block (n = 80, 23%, P less than 0.05). Only one out of 41 DDD paced patients showed AF at follow-up. VVI stimulation seems to favor AF due to retrograde conduction in SSS. Only 3% of patients with SSS developed second- or third-degree AV block. Therefore, atrial pacing is preferable in most patients with SSS.

Aged↗
PubMed1990

Lethal myocarditis with atrioventricular block and ventricular tachycardia--a case report.

This case report details the acute clinical course and the follow-up of a 42-year-old woman with active recurring myocarditis, the main electrical features of which were atrioventricular block and ventricular tachycardia. It also focuses on immunohistological and serological parameters of autoreactivity that might explain the chronic clinical course over a period of 10 years.

Adult↗
PubMed1989

The vascular endothelium as target of humoral auto-reactivity in myocarditis and rejection.

The vascular endothelium plays a key role in immunologic reactions that also involve the heart: Increased expression of class 1 and 2 antigens of the major histocompatibility complex a common finding in acute rejection after heart transplantation whereas in myocarditis this finding is less pronounced. Another form of involvement of the endothelial cells in the secondary immune response has been reported only infrequently; anti-endothelial antibodies, which may be cytolytic to living cultured human endothelial cells, were demonstrated to be bound to the endomyocardial biopsies of patients with different forms of rejection and with biopsy proven myocarditis and circulating in the peripheral blood of the patients as cytolytic autoantibodies.

Autoantibodies↗
PubMed1989

[Diagnosis of extrarenal, secondary forms of hypertension].

The secondary, nonrenal forms of hypertension principally include pheochromocytoma, hyperaldosteronism, hypercortisolism, iatrogenic hypertension following medication, and hypertension related to overindulgence. Other very rare secondary forms of hypertension will not be considered here. Pheochromocytoma is the most dangerous of all the forms of hypertension. Diagnosis of the underlying cause of endocrine-derived hypertension is achieved by hormone analysis. Due to the small size of endocrine tumors, their exact localization can often not be established by sonography, such that CT or MR are the examinations of choice. Scintigrams are only necessary in special cases. For tumor localization in Cushing's disease, hormone measurements from the petrosal sinus are occasionally required. Medication, and above all, continual alcohol consumption, play an increasing role in the etiology of hypertension.

Adrenal Gland Neoplasms↗
PubMed1989

[Validation of indirect myocardial parameters of oxygen consumption in patients with normal and pathologically changed ventricular function].

Five frequently used hemodynamic oxygen consumption parameters were compared with the directly measured myocardial oxygen consumption (MVO2) in 28 patients with different heart diseases (4 without heart disease, 2 with mitral valve prolapse, 20 with coronary artery disease with or without left ventricular dysfunction, 2 with mitral regurgitation, 1 with hypertrophic obstructive cardiomyopathy and 3 with left ventricular hypertrophy due to hypertension). In most patients pressure-rate product (r = 0.908), tension-time index (r = 0.977), triple product (r = 0.970), pressure-work index (r = 0.954) and the additive parameter Et (r = 0.994) correlated relatively close with MVO2 under conditions of normal or low inotropic stimulation. Already during a moderately enhanced contractile state, tension-time index (r = 0.855), triple product (r = 0.873) and pressure-work index (r = 0.906) lose their close correlations with MVO2. Only pressure-rate product (r = 0.933) and Et (r = 0.982) remained reliable predictors of MVO2 also under these conditions of moderate positive inotropic stimulation.

Adult↗
PubMed1988

Vasoconstrictor role of vasopressin and angiotensin in experimental aortic stenosis in the rat.

The roles of vasopressin and angiotensin II in the regulation of peripheral vascular tone were investigated in control rats and in rats with chronic (15 weeks) aortic stenosis, by intravenous application of a specific antagonist to the vascular receptors of vasopressin and the angiotensin-converting enzyme inhibitor teprotide. The application of a Silver clip (0.6 mm) on the aorta ascendens produced a hemodynamically effective aortic stenosis with an increase in left ventricular weight (38%), a reduction in mean arterial pressure, cardiac index, and stroke volume index, and an increase in peripheral vascular resistance. In both groups of rats, a bolus injection of 30 micrograms of the vasopressin inhibitor d (CH2) 5 Tyr (Me) arginine vasopressin (AVP) showed an agonistic effect by increasing arterial pressure by 11 and 15 mm Hg, respectively, and no antagonistic effect in the control animals. In the rats with chronic aortic stenosis we observed a significant fall in blood pressure (4.1 +/- 5.5 mm Hg; p less than 0.05) and a reduction in peripheral vascular resistance of 6.3% (p less than 0.02). Stroke volume index and heart rate did not change. Most of the animals with aortic stenosis had inappropriately elevated plasma levels of vasopressin and increased levels of plasma renin concentration. The rats with aortic stenosis and inappropriately increased values of vasopressin showed significantly lower plasma osmolality, cardiac index, and stroke volume index and increased peripheral vascular resistance compared with the stenosed rats with a normal osmoregulation of vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1988

Course of symptoms and spontaneous ECG in pacemaker patients: a 5-year follow-up study.

We investigated the course of symptoms and the spontaneous ECG retrospectively in 308 patients who had received a pacemaker because of atrioventricular (AV) block (n = 115), sick sinus syndrome (SSS, n = 107), bradyarrhythmic atrial fibrillation (bradyarrhythmia, n = 51), carotid sinus syndrome (CSS, n = 16), complete bifascicular block associated with 1st degree AV block (n = 13) and with other indications (n = 6). The mean implantation time was 63 months. The clinical state of 93% of all patients improved after pacemaker implantation; their symptoms decreased markedly. Persisting syncopy in some patients with SSS, however, supports a restricted implantation policy. We rarely saw improved AV conduction in patients with AV block (11%). Furthermore, in patients with SSS, atrial fibrillation occurred significantly more often (35%) than in those with AV block (17%; P less than 0.01). Only 3% of patients with SSS developed 2nd and 3rd degree AV block within the observation period. In all patients with initial bifascicular block and additional 1st degree AV block, pacing prevented further syncopal attacks; four of them showed 3rd degree AV block at control, indicating that pacemaker implantation is mandatory in symptomatic patients with bifascicular disease and 1st degree AV block.

Adult↗
PubMed1988

Atrial fibrillation and embolic complications in paced patients.

UNLABELLED: Atrial fibrillation (AF) and thromboembolism are discussed to be complications of the VVI mode. We reinvestigated the spontaneous ECG and the anamnesis of 246 pacemaker patients with the indications second and third degree atrioventricular block (AV block, n = lll), sick sinus syndrome (SSS, n = 101) and other indications (n = 34), all had shown sinus rhythm at implantation. The mean implantation time was 63 +/- 45 months (203 VVI and 43 dual chamber pacemakers). THE RESULTS: (1) Atrial fibrillation was found in 63 patients (26%). Only one of them had a DDD pacemaker inserted, the implantation time of dual chamber devices being shorter, however, (2) The incidence of AF in patients with SSS (37%) was significantly higher (P less than 0.01) than in patients with AV block (19%). (3) Three patients suffered from strokes or transitory ischemic attacks in the follow-up, only one of them had AF at control. CONCLUSIONS: Our results confirm that VVI stimulation favors AF long-term which is most likely due to irritation of the atrial rhythm by retrograde conduction. In our patients the incidence of thromboembolic complications was not higher in the group of patients with AF. However, from this study in surviving patients, we cannot exclude that we lost some patients due to severe stroke.

Aged↗
PubMed1988

Cardiovascular effects of AVP and ANG in experimental pulmonic stenosis in rats.

Our objectives were to examine the role of vasopressin and renin in the regulation of peripheral vascular tone in an animal model of right ventricular failure due to chronic (10 wk) pulmonic stenosis. We tested in chronically instrumented conscious control rats and in rats with pulmonic stenosis on a normal and a high-sodium diet both vasoconstrictor systems by applying specific inhibitors. The rats with pulmonic stenosis showed significant hemodynamic changes, a hypertrophy of the right ventricle, increased levels of plasma renin concentration, and inappropriately elevated plasma levels of vasopressin in comparison to control animals. Plasma renin concentration was suppressed in the sodium-loaded controls. After the administration of a specific inhibitor of the vascular receptors of arginine vasopressin [30 micrograms, d(CH2)5Tyr(Me)AVP], we found no hemodynamic changes in control rats on the normal diet, a reduction of mean arterial pressure in the sodium-loaded controls (4 +/- 4 mmHg; P less than 0.005), and in the animals with pulmonic stenosis and normal sodium intake (5 +/- 5 mmHg; P less than 0.001) and high-salt diet (6 +/- 7 mmHg; P less than 0.02). Intravenous bolus injection of teprotide (1 mg/kg) resulted in a decrease of mean arterial pressure in the control group (normal diet) of 9 +/- 8 mmHg (P less than 0.005). The fall of blood pressure (22 +/- 10 mmHg; P less than 0.001) in the rats with pulmonic stenosis was significantly greater (P less than 0.01) and was strongly related to plasma renin concentration. Therefore, vasopressin and the renin-angiotensin system contribute to an increase of peripheral vascular tone in chronic pulmonic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗