[Systolic-diastolic function of the left ventricle and flowmetry of the lower limbs in the treatment of moderate essential arterial hypertension with atenolol-chlorthalidone].
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Biomedical subjects
Publications and source records attributed to G Bisi.
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Clonidine administration by i.v. infusion in 12 patients with hypertension emergencies (diastolic blood pressure over 130 mmHg) resulted in the normalization of blood pressure (BP) in all patients. Lowering of BP was associated with a reduction in total and lower limb vascular resistance. Heart rate showed a slight and brief decrease. Cardiac performance (determined by radionuclide angiocardiography) was improved as indicated by the significant increase of ejection fraction and decrease of both end-diastolic and end-systolic volumes. The dosage of clonidine was progressively increased until a normal BP (mean BP less than or equal to 105 mmHg) was obtained. In all patients a normal BP was achieved and in none was an initial hypertension effect observed. The total mean dose required for control of BP was 382.5 +/- 98.3 micrograms, administered over a mean period of 26.5 +/- 4.6 min. Side-effects, represented by dry mouth and drowsiness, were well tolerated and of short duration. It is concluded that clonidine is an effective and safe alternative in the treatment of hypertensive emergencies.
In order to identify the hemodynamics of borderline essential hypertension, radionuclide angiography was performed before and after bolus injection of furosemide (40 mg i.v.) both at 3 min (i.e. before diuretic effect) and at 30 min (i.e. after diuretic effect) in 16 borderline (B) patients and in 14 age-matched WHO classification I-II essential hypertensives (H) patients. 14 age-matched normotensive (N) subjects were used as controls. B patients were further subdivided into two subgroups according to a cardiac index under or above 3 liter/min/m2 in basal conditions. Baseline hemodynamic characteristics showed higher values of mean arterial pressure (MAP) and systemic vascular resistance index (SVRI) in both H and B patients when compared with N subjects (p less than 0.001). Furthermore, B and H patients exhibited lower values of left ventricular peak filling rate (PFR) than seen in N subjects (p less than 0.01 and p less than 0.05, respectively). H patients demonstrated higher peak systolic blood pressure/endsystolic volume ratio (PSP/ESV) than seen in N subjects (p less than 0.05). PFR positively correlated with peak emptying rate (PER) only in N and B patients (p less than 0.05). After furosemide administration, even though differences were observed in the absolute values, B and H patients showed similar hemodynamic patterns. Only the B subgroup with cardiac index (CI) greater than 3 liter ('volume-dependent' patients) showed a decrease in left ventricular end-diastolic volume index (LVEDVI) at 30 min associated with a lowering of stroke index (SI; p less than 0.005 for both), when compared with pre-drug values. In B patients with CI less than 3 liter ('afterload-dependent' patients) no differences were observed either at 3 min or at 30 min in comparison with values obtained prior to drug administration. Moreover, in this subgroup, like in H patients, there was a negative correlation (p less than 0.01) between 3-min percent change of SVRI and 3-min percent change of SI. Our data suggest that in 'borderline' hypertension: (a) there may be an increase in peripheral resistance, as in established hypertension, especially when age-matched groups are considered; (b) the earliest sign of compromised left ventricular function is the reduction in diastolic PFR but, unlike established hypertension, this index is still correlated with systolic function; (c) cardiac output might be even somewhat reduced and also negatively correlated with vascular resistance ('afterload-dependent' hearts); (d) furosemide (acute administration) might contribute to a better definition of hemodynamic behavior.
Whether physical training, soon after myocardial infarction (MI), has effects upon intrinsic cardiac function at rest and during exertion remains unresolved. We have evaluated ventricular function using radionuclide angiography at rest and during stress testing before and after 3 months' physical training. This has been correlated with the site of MI and with changes in the ST segment during the maximal exercise test performed before the postmyocardial infarction rehabilitation program. We have studied 27 patients, mean age 54 +/- 10 years, in NYHA class I or II. Twelve showed no changes in the ST segment during erogmetric stress test (group 1); seven showed ST segment depression greater than 1 mm in leads different from those of MI (group 2); eight showed ST segment elevation of 2 mm (group 3). Twelve patients had had anterior MI only (AMI group); twelve inferior MI only (IMI group). After rehabilitation, all patients showed an increased work capacity and a decreased double product at the same work load. In the total group, significant increases were found in the left ventricular ejection fraction (LVEF) and in the contractile regional performance (LVwm) at rest, as well as a lesser decrease in the LVEF during handgrip test. Group 1 showed a significant increase in LVEF, associated with a decrease in left ventricular end-diastolic volume (EDV) at rest. Group 2 showed unchanged variables after rehabilitation. Group 3 showed a better LVEF during handgrip with an increase of EDV at rest. The AMI group showed a better LVEF and LVwm at rest and a better LVEF during handgrip. IMI group showed a better right ventricular ejection fraction during handgrip without improvement in LVEF. No patient with IMI had septal asynergy. We conclude that the effects of rehabilitation were linked to the site of MI and to the functional dynamic status of both ventricles.
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Carbochromen increases coronary flow and cardiac output. A previous study has advanced the hypothesis that the latter may be due to afterload reduction. Fourteen patients with coronary heart disease have now been studied by means of radionuclide angiocardiography. Gated blood pool angiocardiographic data were collected in basal conditions and, without moving the patient, 80 mg of carbochromen were administered i.v. Data were collected again, following infusion, during 3'-6'(1) and 7'-10'(2) periods. Changes in the following parameters have been evaluated: LV ejection fraction (EF), LV ejection rate (ER), system pressure (BP), heart rate (HR), cardiac output index (CO), stroke volume index (SV), LV end-diastolic volume index (EDV), systemic vascular resistance index (SVR), regional LV wall motion. During period 1 a significant decrease was observed in BP and SVR, the other parameters remaining unchanged. During period 2 there was a significant increase in CO, SV, EF, ER and a significant decrease in SVR. BP was unchanged. No changes were ascertained in HR and EDV. Eight patients, in basal conditions, showed asynergy in the LAO projection. Three of these patients showed improved wall motion during period 2. A possible central action of carbochromen should be pointed out. This conclusion can be drawn by observing the increase in the pump indexes, while BP and SVR show a decrease and EDV and HR no change. The left ventricular wall motion improvement observed in some of the cases confirms the possibility that carbochromen is capable of improving cardiac contractility. This effect may follow the regional myocardial perfusion increase.
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Factors influencing the anterior systolic movement of the aortic posterior wall (PAM) are complex and still controversial. Left atrial events seem to be more important that stroke volume or left ventricular function in determining PAM. Even if the reduction of systolic aortic movement is generally associated to a severe impairment of left ventricular function, very few studies correlate the changes in the amplitude of aortic systolic movement to the hemodynamic pattern. In 50 patients posterior aortic wall echocardiograms, right heart catheterization and 99mTc angiocardiography were performed within 24 h. According to hemodynamic and left ventricular wall motion parameters 18 patients resulted to have a normal (1st group) and 32 patients (2nd group) an impaired left ventricular function. In the 2nd group mean values of PAM were significantly lower than in the 1st group (7.4 +/- 2.9 mm vs 10.2 +/- 1.9 mm). A significant correlation was found between PAM and hemodynamic parameters, i.e. CPW (r = 0.58), EF (r = 0.58) and SV (r = 0.40), whereas no significant correlations were found between these parameters and left atrial dimensions and between PAM and left atrial dimensions. A high significant correlation was found between PAM and echocardiographically measured septal wall motion (r = 0.80). All patients with PAM Less Than 6 mm and echo septal wall motion Less Than 5 mm had an akinesis or a dyskinesis of septal wall quantitatively determined with 99mTc angiocardiography. These findings suggest that one of the main determinants of PAM is left ventricular wall motion and in particular left ventricular septal motion.
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A radioisotopic technique which, through the injection of 99mTc-red cell into the pulmonary artery, gives images of left ventricular chamber in RAO at first pass and in LAO at blood pool gated, has been assessed. A quantitative analysis of left ventricular wall motion was performed with semiautomatic program. The Authors report their experience with 42 patients.
A radioisotopic technique which, through the injection of 99mTc-red cell into the pulmonary artery, gives images of left ventricular chamber in RAO at first pass and in LAO at blood pool gated, has been assessed. A quantitative analysis of left ventricular wall motion was performed with semiautomatic program. The Authors report their experience with 30 CHD patients.
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