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Biomedical subjects

M Karcz

Publications and source records attributed to M Karcz.

2 recordsLinked to original sources

Left ventricular outflow tract gradient decrease with non-surgical myocardial reduction improves exercise capacity in patients with hypertrophic obstructive cardiomyopathy.

OBJECTIVES: This study was undertaken to evaluate mid-term clinical results of non-surgical myocardial reduction in patients with hypertrophic obstructive cardiomyopathy. METHODS: Twenty-five patients with left ventricular outflow tract obstruction (mean gradient of 84. 54+/-31.38 mmHg) and symptoms of dyspnoea, angina and/or syncope were treated with non-surgical myocardial reduction. The patients were followed-up for a mean period of 10.44+/-1.8 months. In all patients clinical examination with echocardiography was repeated after every 3 months of follow-up, and a symptom-limited treadmill test was repeated at the 6 month follow-up. Eighteen patients underwent simultaneous respiratory gas analysis. RESULTS: Clinical follow-up examinations were achieved in all 25 patients. Persistent left ventricular outflow tract gradient reduction was seen in 23 patients. Seventeen patients had a reduction of left ventricular outflow tract gradient >50% of baseline value. Twenty patients showed a clinical improvement from 2.8+/-0.5 up to 1.2+/-0.5 NYHA class (P<0.001). The clinical improvement was matched by an improvement in objective measures of exercise capacity in patients with significant left ventricular outflow tract gradient reduction. Exercise time increased from 571.9+/-192.2 to 703.5+/-175.4 s, P<0. 001, and peak VO(2)increased from 14.6+/-5.2 to 20.5+/-8.6 ml. kg(-1)min(-1), P<0.05. CONCLUSION: Significant left ventricular outflow tract gradient reduction with exercise capacity improvement was achieved in the majority of patients treated with non-surgical myocardial reduction. We recommend this method as an alternative to surgery for symptomatic patients with hypertrophic obstructive cardiomyopathy.

Cardiac Catheterization↗

Striatal and nucleus accumbens D1/D2 dopamine receptors in neuroleptic catalepsy.

Haloperidol (2.5-10 micrograms) injected bilaterally into the ventro-rostral striatum or into the nucleus accumbens induced dose-dependent catalepsy whereas its injection into the dorso-rostral striatum (2.5 micrograms) was ineffective. Similarly, the specific antagonist of D1 receptors, SCH 23390 (1-5 micrograms), injected into the ventro-rostral striatum or nucleus accumbens, as well as the specific antagonist of D2 receptors, sulpiride, injected into the ventro-rostral striatum (0.02-15 micrograms) or nucleus accumbens (1-15 micrograms), induced a dose-dependent catalepsy. Both drugs (SCH 23390 2 micrograms, sulpiride 0.5 micrograms) were ineffective when injected into the dorso-rostral striatum. Doses of sulpiride about 100 times lower than those injected into the nucleus accumbens were sufficient to evoke an equipotent catalepsy when injected into the ventro-rostral striatum. However, similar doses of haloperidol and SCH 23390, injected into the ventro-rostral striatum and nucleus accumbens, evoked a similar catalepsy. It is concluded that (1) the catalepsy induced by systemic administration of haloperidol seems to result from the action of this drug on both the ventro-rostral striatum and the nucleus accumbens, (2) both D1 and D2 dopamine receptors in the ventro-rostral striatum are involved in the cataleptogenic action of neuroleptics, and (3) in the nucleus accumbens, only D1 dopamine receptors seem to play an important role in this phenomenon.

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