[Hypertrophy and left ventricular function following angiotensin-converting enzyme inhibition in hypertensive patients. Echocardiographic analysis].
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Biomedical subjects
Publications and source records attributed to G Grenci.
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In order to assess the reliability of Doppler echocardiography in the determination of mean mitral gradient 38 consecutive patients (pts) affected by rheumatic mitral valve stenosis (MS) were analyzed by continuous wave Doppler echocardiography (CWD). Cardiac catheterization (CATH) was performed within 24 hours from echocardiographic examination. The mean diastolic mitral gradient (MG) at CATH was calculated by planimetry from simultaneously recorded left ventricular and pulmonary artery wedge pressure. The maximal velocity profile through the mitral valve was used to calculate pressure gradient by CWD. A mean mitral gradient was calculated for each patient by the planimetered velocity profile throughout diastole. MG determined by CATH ranged from 6 to 31 mmHg (mean 15.2 +/- 6.0); MG determined by CWD ranged from 4 to 18 mmHg (mean 10 +/- 3.7). The correlation between CWD and CATH by linear regression analysis was: y = 0.53 X + 1.8; r = 0.85; p less than 0.001. Mean % error of CWD in the assessment of MG was 34.7%. In conclusion this study indicates that CWD seems systematically underestimate MG with respect to CATH. The identification of CWD flow tracings "optimal" for analysis could not represent the maximal velocity of transmitral jet, which is a complex three dimensional entity. In addition non-simultaneous determinations of gradient and day-to-day variations in cardiac output may account for discrepancies between CWD and CATH measurements.
16 patients suffering from hypertension and angina pectoris (class II according to the NYHA) are treated with 100 mg atenolol once daily for three weeks. A good decrease of the blood-pressure values and a clinical improvement of the anginous symptomatology are observed. The bicycle ergometer exercise test showed an increase of the effort tolerance. The addition of 30 mg nifedipine for other three weeks, decreased further on the values of the blood-pressure and of the double product. The ergometric exercise showed an increase of total work and of the maximum working capacity reached by patients. This association (atenolol + nifedipine) was particularly useful in patients who presented symptoms of intolerance toward other drugs (nitroderivate f. es.), because of less collateral effects and easy administration.
The modifications of systolic times during isometric exercise (hand-grip) are evaluated in a group of patients with essential hypertension. In these patients the hand-grip showed a reduction of the PEP, ICT and LVET: the re-establishment of the basal values of the PEP, ICT and LVET, became in variable times and in different ways with regard to the modifications of the miocardial performance induced by hypertension, unlike normal patients, in whom that becomes normally during the period of recovery. Little modifications of the PEP/LVET ratio, are observed in all patients and this ratio is like that observed toward blood-pressure during exercise. Blood-pressure, like heart rate, increased suddenly during exercise and returned on the basal values during the recovery, normally both in the control group and in patients with hypertension arised recently; more slowly and incompletely in patients with hypertension arised long before. The Authors related this fact to the adjustment alterations of the blood pressure.
The clinical effects, the exercise test answer, the left ventricular function by polygraphyc test after administration at middle term of Metoprolol and Labetalol have been evaluated in 20 patients with moderate and non complicated essential hypertension. The study was a double blind cross-over between Metoprolol and Labetalol (270 mg/die per os). Both drugs induced a reduction of PAOS and PAOD. The exercise test induced in all patients a decrease of PAOS and PAOD, showing an improvement of strain tolerance. The normalization of PEP and non modification of LVET seem to confirm that the treatment with Metoprolol and with Labetalol, neither induces significant modification of left ventricular function.
10 patients with systemic essential arterial hypertension have been treated with 200 mg/die of Metoprolol. The systolic times have been valued before and after the treatment. It has been observed a reduction of the pre-ejection period simultaneously and proportionally to the reduction of the arterial pressure and the cardiac frequence. These last parameters and the indices of consumption of oxygen and heart frequence have undergone a significant decrease since the first week of therapy. The bloodless indices which express the myocardic contractility demonstrated instead not to be particularly influenced.
Systolic time intervals are evaluated by polygraphic method in a group of patients with systemic arterial hypertension. An increase of pre-expulsion period (P.E.P.) was found by relative increase of isometric contraction time (I.C.T.) in subjects with "old" hypertension; no significative differences and found in subjects with recent hypertension and in controls. The A. have attributed this alterations to a compensation mechanism of the left ventricle that extends the time of its internal pressure increase to win the resistence of excessive pressure being in aorta, that influences the after load value. According to the Authors', in absence of left ventricular insufficiency, that alteration is not accompanied by other significant mechanocardiographic modifications.
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In a group of patients with previous myocardial infarction S.T.I. are evaluated by polygraphic method. In all examined patients an increment of Pre ejection period (PEP) has been observed caused by the increase of the Deformation time (Q-S1). Increased values of SFW/RFW ratio are observed in dyastolic phase. The Authors, in absence of other meccanocardiographic alterations, have ascribed the anomaly to the alteration of the myocardial contraction because of previous necrosis.
Four new cases of Kawasaki Syndrome are presented. The Authors discuss the etiopathogenetic hypothesis, point out the usefulness of treatment with ASA + high dose intravenous gammaglobulins, underline the risk of cardiac complication.