Biomedical subjects

P Kenedi

Publications and source records attributed to P Kenedi.

At least 19 recordsLinked to original sources

PubMed1999

Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension

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Journal Article↗

PubMed1998

Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension.

BACKGROUND: Left ventricular hypertrophy (LVH) represents an independent risk factor in patients with essential hypertension. Because reversal of LVH may be associated with an improvement of prognosis, the influence of new antihypertensive compounds, such as angiotensin II AT1 receptor antagonists, on LVH should be determined. METHODS AND RESULTS: In a randomized, double-blind trial, 69 predominantly previously untreated hypertensive patients with echocardiographically proven LVH, ie, left ventricular mass index (LVMI) >134 g/m2 in men and >110 g/m2 in women and/or end-diastolic septal thickness >12 mm, received either the angiotensin II antagonist valsartan or atenolol for 8 months. Echocardiographic data of 58 patients were available. After 8 months of valsartan treatment (n=29), LVMI decreased from 127+/-23 to 106+/-25 g/m2 (ratio [R]=0.83; 95% CI, 0.79 to 0.87; P<0.0001 versus baseline). Under atenolol (n=29), LVMI decreased to a smaller extent, from 127+/-25 to 117+/-27 g/m2 (R=0.92; 95% CI, 0.86 to 0.98; P=0.0082 versus baseline). The mean reduction of LVMI came to 21 g/m2 under valsartan and only to 10 g/m2 under atenolol (R=0.91; 90% CI, 0.85 to 0.97 versus atenolol). Baseline mean blood pressure values were determined to be 163+/-12/101+/-6 mm Hg before treatment with valsartan and 160+/-14/103+/-6 mm Hg before atenolol treatment. After 8 months of treatment, mean blood pressure decreased to 146+/-13/90+/-7 mm Hg with valsartan and to 147+/-18/90+/-7 mm Hg with atenolol. Nine patients in the valsartan group and 8 patients in the atenolol group required additional medication with hydrochlorothiazide. CONCLUSIONS: Antihypertensive treatment with the angiotensin II antagonist valsartan for 8 months produced a significant regression of LVH in predominantly previously untreated patients with essential hypertension. The drug may be safely administered in this subset of hypertensive patients; however, the long-term benefit in terms of risk reduction has still to be evaluated in further trials.

Angiotensin II↗

PubMed1996

Influence of isradipine and spirapril on left ventricular hypertrophy and resistance arteries.

Left ventricular hypertrophy is a common clinical feature in hypertensive patients and may be associated with structural changes in vessel morphology. In an open prospective trial, we evaluated 14 patients with previously untreated hypertension (163 +/- 2/104 +/- 2 mm Hg) and an echocardiographically determined left ventricular mass index of 141.6 +/- 5.2 g/m2, indicating left ventricular hypertrophy. We obtained a gluteal skin biopsy sample before starting treatment to investigate subcutaneous small-artery (approximately 200 to 400 microns diameter) morphology and function. Patients then received antihypertensive treatment with a combination of spirapril (3 or 6 mg) and isradipine (2.5 or 5 mg). Echocardiographic recordings were made after 6 months and 1 year, and a final biopsy was taken after 1 year. After 1 year, blood pressure was significantly reduced to 142 +/- 3/ 90 +/- 1 mm Hg (P < .001), and left ventricular mass index decreased significantly to 105.3 +/- 5.8 g/m2 (P < .001). Baseline media-lumen ratio (7.64 +/- 0.48%) was not markedly reduced (7.21 +/- 0.55%), although a decrease occurred in 7 of 12 evaluable patients. Norepinephrine-induced vasoconstriction was markedly reduced after 1 year. In conclusion, a significant regression of left ventricular hypertrophy was obtained after 1 year of treatment with spirapril and isradipine, whereas a similar reduction in medial thickness relative to lumen diameter of subcutaneous small arteries could not be observed in all patients. Reversal of structural changes in resistance vessels may require a longer treatment period in patients with proven left ventricular hypertrophy.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1993

[Nitroglycerin in comparison with nifedipine in patients with hypertensive crisis].

To determine whether nitroglycerin is just as effective as nifedipine in lowering the blood pressure in excessive hypertension and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg of nitroglycerin sublingually or a 10 mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mm Hg to 171/95 mm Hg and after nifedipine from 210/118 to 185/102 mm Hg. The greater effect of nitroglycerin results from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15 to 20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mm Hg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant difference in side-effects was determined. Since a hypertensive crisis is usually accompanied by left-ventricular failure, pulmonary edema or angina pectoris and infarction, and nitroglycerin has been definitively shown to positively influence these conditions, preference should be given to nitroglycerin in the treatment of hypertensive crisis.

Administration, Oral↗

PubMed1992

Comparison of nitroglycerin with nifedipine in patients with hypertensive crisis or severe hypertension.

To determine whether nitroglycerin is as effective as nifedipine in lowering the blood pressure in severe hypertension and hypertensive crisis, two groups of 20 patients received in random sequence either 1.2 mg nitroglycerin sublingually or a 10-mg nifedipine capsule, which was chewed and swallowed. The blood pressure fell after 5 min in the nitroglycerin group from 211/122 mmHg to 171/95 mmHg and after nifedipine from 210/118 to 185/102 mmHg. The greater effect of nitroglycerin may result from faster absorption through the oral mucosa than through the small intestinal mucosa where nifedipine is primarily absorbed. After 15-20 min a satisfactory reduction in blood pressure was reached in both groups: 157/91 and 158/92 mmHg, respectively. After 30 min the heart rate in the nitroglycerin group had decreased from 83 to 80/min, but in the nifedipine group it had increased from 84 to 90/min. The reduction in blood pressure persisted up to 6 h. No significant differences in side effects were determined. Since a hypertensive crisis is usually accompanied by left ventricular failure, pulmonary edema, angina pectoris, or infarction, nitroglycerin has been definitively shown positively to influence these conditions, and preference should be given to nitroglycerin in the treatment of hypertensive crises.

Acute Disease↗

PubMed1987

Dose-effect relationship amongst three different sustained-release forms of isosorbide 5-mononitrate in patients with coronary artery disease.

Fifteen patients with coronary artery disease and stable angina pectoris were included in a double-blind, randomized, cross-over study. The patients received 25, 50 and 100 mg isosorbide 5-mononitrate, as well as a placebo, for subsequent 1-week periods. On the 7th day of each treatment period, 8 h after medication application, an exercise test was performed. A highly significant (p less than 0.001) and dose-dependent reduction of the sum of the ST-segment depression was observed at similar workloads: 28.6, 46 and 63.5% decreases occurred at the 25, 50 and 100 mg isosorbide 5-mononitrate doses, respectively. Compared to placebo, the frequency of anginal attacks and the consumption of nitroglycerin likewise decreased highly significantly (p less than 0.001) with all three doses. Isosorbide 5-mononitrate plasma levels (8 h post-application) increased linearly with the dose; amounting to 228 +/- 53, 485 +/- 93 and 991 +/- 177 ng/ml at the 25, 50 and 100 mg doses of the sustained release medication forms, respectively.

Aged↗

PubMed1986

[Intraindividual dose-response relationship of sustained-release Elantan].

Fifteen patients with coronary artery disease and stable angina pectoris were included in a double-blind, randomized, cross-over study. The patients received 25, 50 and 100 mg isosorbide-5-mononitrate, as well as a placebo, for subsequent one week periods. On the 7th day of each treatment period, 8 h after medication, an exercise test was performed. A highly significant (p less than 0.001) and dose-dependent reduction of the sum of the ST-segment depression was observed at similar work loads: 28.6%, 46% and 63.5% decreases occurred with the 25, 50 and 100 mg isosorbide-5-mononitrate doses, respectively. Compared to placebo, the frequency of anginal attacks and the consumption of nitroglycerin also decreased highly significantly (p less than 0.001) with all three doses. Isosorbide-5-mononitrate plasma levels (8 h post-application) increased linearly with the dose; amounting to 228 +/- 53, 485 +/- 93 and 991 +/- 177 ng/ml at the 25, 50 and 100 mg doses of the sustained-release medication forms, respectively.

Aged↗

PubMed1983

Antianginal efficacy of long-term nitrate therapy.

Forty patients suffering from angiographically proven coronary artery disease with stable angina pectoris were subjected to a randomized, double-blind, placebo-controlled study. The patients were divided into three groups who for 28 days running were given 20, 40, or 60 mg ISDN respectively, in sustained-release form, three times a day, and one group which received a placebo. A bicycle exercise test was performed prior to and 1, 3, 5, and 8 h following drug administration. The acute study was repeated at 14 and 28 days after drug administration. Following acute administration of 20, 40, or 60 mg ISDN SR a significant reduction in ST-segment depression was observed; between the ISDN-treated groups and the placebo group the difference was significant. After 4 weeks of treatment the mean reduction in ST-segment depression was unchanged. There was a significant improvement in the frequency of anginal attacks in all the ISDN-treated groups after 4 weeks of treatment, but not change in the placebo group. Thus, no attenuation of the anti-ischemic and antianginal effect could be recorded. During acute administration there was a significant dose-dependent reduction in blood pressure at rest in the ISDN-treated groups as compared with the placebo group. After 4 weeks of treatment a considerable attenuation of the blood pressure reduction was noted in all the ISDN-treated groups. Heart rate and pressure-rate product did not reflect any uniform trend.

Angina Pectoris↗

PubMed1982