Effect of enalapril on left ventricular mass and performance in essential hypertension.

The effect of enalapril on left ventricular (LV) morphology and function was studied in 12 hypertensive patients. The subjects were evaluated after 2 weeks of placebo and after 4 months of treatment with enalapril (20 or 40 mg once daily), using M-mode digitized echocardiograms. The drug reduced arterial blood pressure in all patients. Systemic vascular resistance decreased significantly without changes in cardiac output and heart rate. No patient had significant side effects. After treatment LV mass decreased significantly (233 +/- 46 to 204 +/- 37 g, p less than 0.01); the reduction was due to a decrease in septal and posterior wall thickness, without changes in LV diameter. LV systolic function remained unchanged, whereas peak lengthening rate of LV dimension, an index of LV diastolic function, increased significantly (4.05 +/- 1.8 to 5.11 +/- 1.8 s-1, p less than 0.01). After treatment the basal inverse correlation between peak shortening rate and wall stress did not change, the inverse correlation between peak lengthening rate and wall stress became closer and the basal inverse correlation between peak lengthening rate and LV mass disappeared. In conclusion, antihypertensive treatment with enalapril led to a significant regression of LV hypertrophy associated with improvement in LV diastolic performance and no deterioration of LV systolic function.

Double-blind comparison of perindopril and captopril in hypertension. Effects on left ventricular morphology and function.

Using digitized M-mode echocardiograms, we compared, in a double-blind study, the effects of 4 to 8 mg perindopril given once daily and 25 to 50 mg captopril given twice daily on the left ventricle (LV) in 20 hypertensive patients. Both treatments significantly (P less than .001) lowered blood pressure, reducing systemic vascular resistances. After 3 months both drugs induced a comparable percentage of reduction in LV mass, with an increase in the peak rate of LV relaxation and no changes in the peak rate of LV contraction. Our results demonstrate that perindopril once daily is an effective antihypertensive agent; it is also able, like captopril, to induce regression of LV hypertrophy, with improvement in diastolic performance and no deterioration in ventricular systolic function.

Improved left ventricular function after short-term treatment with fructose-1,6-diphosphate: echocardiographic study in chronic ischemic heart disease and idiopathic dilated cardiomyopathy.

The effect of fructose-1,6-diphosphate (FDP) on left ventricular function was assessed in seven patients with chronic ischemic heart disease and eight patients with idiopathic dilated cardiomyopathy. In a crossover study design each patient received 10 gm of FDP or saline placebo intravenously for three days. An M-mode echocardiographic assessment of left ventricular (LV) function was made before and after each treatment period. After FDP treatment, LV end-diastolic and systolic dimensions showed a 6% reduction (P less than 0.01), while peak lengthening rate of LV dimension in diastole and peak shortening rate of LV dimension in systole increased 17% and 10%, respectively (P less than 0.05). There was evidence that FDP was more effective in the patients with ischemic heart disease than in the patients with cardiomyopathy.

Computerized echocardiographic study of left ventricular function and cardiodynamic investigation with a new antihypertensive agent (indenolol).

Indenolol hydrochloride is a recently introduced antihypertensive substance. Although it has beta-adrenoceptor blocking activity, its action is due to total peripheral resistance reduction. We investigated the effects of indenolol therapy on left ventricular performance in 15 patients with essential hypertension. Assessments were made using systolic time intervals and computerized echocardiography. The echocardiographic and mechanocardiographic tracings were recorded three times: at the beginning of the trial, after seven days of placebo, and after three weeks of indenolol treatment. The indenolol therapy significantly decreased (P less than 0.001) systolic and diastolic blood pressures and heart rate in all patients, both in supine and standing positions. After three weeks of treatment, systolic time intervals and echocardiographic determinants of left ventricular function were substantially unchanged in comparison with the basal and placebo evaluations. We conclude that indenolol exerted a marked effect on chronotropism but no demonstrable negative effect on inotropism in patients with essential hypertension. No clinical signs of heart failure were recorded. Side effects were absent, and patient compliance was good in all cases.

Mitral valve prolapse in systemic lupus erythematosus.

Despite a low incidence of clinical manifestations, autopsy data suggest endocardial and myocardial disease in about 50% of patients with systemic lupus erythematosus. To investigate whether mitral valve prolapse can be considered a clinical manifestation of cardiac involvement in systemic lupus erythematosus, we carried out an echocardiographic study in 51 affected subjects and 102 normals matched for age and sex. Prevalence of mitral valve prolapse was 25% in patients with systemic lupus erythematosus and 9% in healthy controls with a statistically significant difference (p less than 0.01). Neither pericardial effusion nor prolonged (more than 12 months) treatment with corticosteroids were associated with higher prevalence of mitral valve prolapse. Libman-Sacks verrucae on the mitral valve apparatus as well as focal myocardial scars affecting the papillary muscles and adjacent myocardium could be responsible for the development of the valvular dysfunction. We suggest that mitral valve prolapse can be considered a manifestation of cardiac involvement in patients with systemic lupus erythematosus.

Kinetocardiographic detection of ventricular dyssynergy after myocardial infarction. Correlations with two-dimensional echocardiography.

The aim of this study was to determine if kinetocardiography can detect regional abnormalities of left ventricular kinetics, as occurs in coronary patients. Kinetocardiogram, M-mode and two-dimensional echocardiograms were recorded in 33 subjects (mean age 63, range 29-75 years), who previously had a myocardial infarction. On two dimensional echocardiograms, long axis, short axis, apical 4-chamber and apical 2-chamber projections were studied. Regional contractile abnormalities were rated as hypokinesis, akinesis, dyskinesis and aneurysm. In 6 subjects two dimensional echocardiogram was normal, in 5 it showed hypokinesis with left ventricular normal dimension or dilatation, and in the remaining 22 patients various regional kinetic abnormalities were observed. The kinetocardiogram showed paradoxical systolic movements in all patients with ventricular dyssynergy and was normal in all patients with normal ventricular kinetics, with or without left ventricular dilatation and global hypokinesis. There were no correspondences between echocardiography and kinetocardiography, regarding sites and amount of abnormalities. Kinetocardiography can thus noninvasively detect qualitative left ventricular kinetics abnormalities, in patients with myocardial infarction.

[Obesity and the heart]. / Obesità e cuore.

Obesity has been identified as an independent risk factor for coronary heart disease and congestive heart failure. Although congestive heart failure can be secondary to coronary heart disease, in morbid obesity these conditions can be independent. Cardiac structure and function can be altered even in the absence of systemic hypertension and underlying organic heart disease. In obese patients total blood volume increases and creates a high cardiac output state that may cause ventricular dilatation and ultimately eccentric hypertrophy of the left (and possibly the right) ventricle. Eccentric left ventricular hypertrophy produces diastolic dysfunction. Systolic dysfunction may ensue due to excessive wall stress if wall thickening fails to keep pace with dilatation. This disorder is referred to as obesity cardiomyopathy. The frequent coexistence of systemic hypertension in obese individuals facilitates development of left ventricular dilatation and hypertrophy. Congestive heart failure may occur and may be attributable to left ventricular diastolic dysfunction or to combined diastolic and systolic dysfunction. The risk of coronary heart disease seems to be more strictly correlated to central obesity than to increased body mass index. Insulin resistance seems to be the key factor that links obesity and ischaemic heart disease. In such a condition the so called Syndrome X appears. It is characterized by: obesity, systemic hypertension, diabetes mellitus, hypertriglyceridaemia and reduced HDL cholesterol levels. Considering that left ventricular hypertrophy is often present, many risk factors coexist in obese patients. Weight loss is very useful in obese patients. It may reduce mortality and morbidity for coronary heart disease and delay or avoid the appearance of congestive heart failure. It is proved that after weight loss, blood pressure, glucose, cholesterol, triglycerides and left ventricular mass decrease.

Effect of indenolol treatment on beta-adrenergic receptors of polymorphonucleates in essential hypertension.

Indenolol is a new antihypertensive agent, whose beta 1-adrenoceptor antagonist properties combined with beta 2-adrenoceptor agonist properties have been shown by experimental studies in animals. Our previous work reported that in vivo beta-adrenoceptor blocking drugs markedly increase the beta-adrenoceptor (BAR) number, without increasing BAR affinity. The aim of this study was to evaluate BAR density and affinity before and after indenolol therapy in membranes of polymorphonucleates (PMN) of patients with essential hypertension. Polymorphonuclear binding parameters were studied in 12 hypertensives (WHO stages I and II) after 14 days of placebo and after 21 days of indenolol therapy (120 mg once daily orally). Indenolol did not increase BAR number but significantly decreased (P less than 0.01) BAR affinity. On the basis of these data it is concluded that indenolol does not induce the same changes in PMN's BAR as previously observed with oxprenolol, propranolol and labetalol. This phenomenon may account for the absence of rebound effect after withdrawal of indenolol in hypertensives.

[Regression of left ventricular hypertrophy in obese hypertensive patients treated with diet and pharmacologic therapy]. / Regressione dell'ipertrofia ventricolare sinistra in ipertesi obesi trattati con terapia farmacologica e dietetica.

Thirty-five obese (Body Mass Index: BMI > 30) hypertensive (diastolic blood pressure > 100 mmHg) patients were studied for 6 months. 18 patients (10 males, mean age 52 +/- 6 years) were treated with captopril 50 mg b.i.d. (Group 1); 17 patients, matched by age, sex and BMI were treated with captopril 50 mg b.i.d. and hypocaloric diet (Group 2). During follow-up a good control of blood pressure levels (< 150/90 mmHg) and a significant reduction in body weight (> 10%) were achieved in all patients of Group 2. Left heart anatomy was accessed by 2D guided M-mode echocardiogram before starting treatment and after 6 months. In Group 1 Interventricular Septal Thickness (ST), Posterior Wall Thickness (PWT) and Left Ventricular Mass (LVM) decreased significantly (p < 0.01). In Group 2 not only ST, PWT and LVM decreased significantly (p < 0.01 for ST and PWT, p < 0.001 for LVM), but also left atrial dimension (p < 0.05) and left ventricular diastolic dimension (p < 0.01). The percent reduction in AD, LVDD and LVM was significantly higher (p < 0.01) in Group 2. In obese hypertensives relevant weight loss can improve the effect of captopril treatment on left ventricular hypertrophy; the decrease of AD and LVDD is probably secondary to a reduction of the volume overload present in obese patients.

Echocardiographic features of hypertensive-diabetic heart muscle disease.

Computerized M-mode echocardiography was used to evaluate left ventricular anatomy and function in 20 patients with hypertension and diabetes mellitus, without signs of overt heart disease. A similar study was performed in 20 patients with hypertension of similar severity and duration and in 20 normal subjects. Mean posterior wall thickness and mean septal thickness were increased in hypertensive patients compared to normal (p less than 0.001), but diabetic patients had thicker septa with respect to nondiabetics (p less than 0.05). All hypertensive-diabetic patients had reduced peak lengthening rate and/or peak velocity of posterior wall thinning. Six of them also had reduced peak Vcf and/or peak velocity of posterior wall thickening. Only 9 of the 20 patients with hypertension alone had abnormal diastolic function; 4 out of these 9 also had abnormal systolic function. We conclude that diabetes causes more severe impairment of left ventricular function in patients with a similar degree of hypertension. The more consistent abnormalities are reduced rate of dimension increase during filling and slower wall thinning, suggesting impaired left ventricular relaxation and distensibility.

Imbalance of heart rate regulation in cluster headache as based on continuous 24-h recordings.

An altered autonomic balance is considered to be a pathogenetic factor in cluster headache syndrome, although there is varying data on sympathetic and/or parasympathetic activation during attacks and/or attack-free intervals. The aim of the present study was to evaluate the day/night pattern of heart rate during the active and remission phases of cluster headache. In addition, the relationship between heart rate changes and the site of pain was investigated to determine if an autonomic imbalance was related to the lateralization of pain. Thirty-nine patients (34 with primary episodic cluster headache and five with primary chronic cluster headache and 30 healthy controls underwent 24-h Holter ECG recording. Nine cluster headache patients were monitored during both phases of the disease. The data obtained confirmed the existence of a disordered chrono-organization in cluster headache (phase-shift of approximately 1 h of heart rate rhythm during the cluster period) together with a low heart rate variability and a higher occurrence of arrhythmias in cluster headache patients with right-sided pain. Differences were also observed in the cluster headache patients when headache free, excluding the pain itself as a reason for the abnormality. The chronobiological data point out a transient rhythmic dysfunction, while heart rate variability changes, mostly related either to the phase of the disease or to the site of pain, probably reflects a central, site-related, dysfunction of the autonomic nervous system in cluster headache.

Partial epileptic seizures of different origin variably affect cardiac rhythm.

PURPOSE: The present study was aimed at evaluating electrocardiographic (ECG) changes associated with partial epileptic seizures without seizure activity secondarily generalized. METHODS: We assessed heart rate (HR) changes occurring during 100 partial epileptic seizures, as recorded by ambulatory EEG-ECG in 50 outpatients. Consecutive R-R intervals were measured for the 30 s immediately preceding the onset and for the first 10-s period of discharge. In addition, HR was sampled at 10-s intervals during EEG paroxysmal discharge and for 1 min after the end of discharge. RESULTS: The highest and lowest respective HR peaks achieved during these seizures were 186 and 44 beats/ min. Analysis of the R-R intervals during the first 10-s period of EEG discharge showed a significant early HR increase in 49% of the seizures; the corresponding figure for an early HR reduction was 25.5%. Eighty percent of the seizures showing an early HR decrease were of temporal lobe origin. No severe cardiac arrhythmias were noted during the seizures. CONCLUSIONS: Our data suggest that an early HR decrease is more probable in temporal lobe seizures than in seizures of other origin. An accurate HR measurement, focused on discharge onset, may provide both a reliable way of evaluating the possible effect of partial seizures on HR and valuable information about the cerebral sites involved in the control of cardiac rhythm.

[Functional anatomy of the left ventricle in hypertensive subjects. Correlations with the clinical severity of hypertension]. / Anatomia funzionale del ventricolo sinistro in soggetti ipertesi. Correlazioni con la gravità clinica dell'ipertensione.

Using computerized M-mode echocardiography we have investigated 58 hypertensive subjects in order to assess whether a correlation could be demonstrated between left ventricular changes induced by hypertension and age of the patients, the duration and severity of hypertension, and damage to other target organs. Various morphological changes of the left ventricle were detected: 14 patients (24%) had concentric hypertrophy of the left ventricle, 12 (20%) had asymmetric septal hypertrophy, 5 (8%) had dilated left ventricle without hypertrophy. Left ventricular mass was increased, when compared to normal controls in 24 patients (41%). With respect to functional abnormalities, the peak lengthening rate of left ventricular dimension in diastole was decreased (+dD/dt less than s-1) in 25 patients (43%). Eight of these patients (14%) also had depressed peak shortening rate of left ventricular diameter in systole (-dD/dt less than 1.9 s-1). Hypertensive retinopathy was present in 23 patients (39%) and impairment of renal function in 8 (14%). Left ventricular mass and systolic and diastolic parameters of left ventricular function did not correlate significantly either with the age of the patients, or with the duration and severity of hypertension, or with the damage present in target organs other than the heart. Left ventricular mass was inversely correlated with the index of left ventricular relaxation (r = -0.53; P less than 0.001), whereas neither the latter nor left ventricular mass were correlated with peak systolic stress. Instead, peak systolic stress was inversely correlated with peak shortening rate of left ventricular diameter, an index of systolic function (r = -0.50; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of age and sex on left ventricular anatomy and function in normals.

Using digitized M-mode echograms, we evaluated the influence of sex on age-related changes of left ventricular (LV) anatomy and function in a normal population (75 males and 75 females, subdivided in age groups for each decade from 20 to 70 years). Aging is accompanied with an increase in septal and wall thickness in both males and females and in LV diameter only in males, with a progressive increase of LV mass more pronounced in males than in females. As regards LV function we found a progressive slowing of relaxation in females and of both contraction and relaxation in males, not related to changes in LV mass.

Measuring left ventricular dimensions by conductance catheter in the rabbit.

A miniaturized (3.5 F), six-electrode conductance catheter was tested in 18 anaesthetized adult rabbits (weight 3.8-4.6 kg, ethylurethane 2.5 g kg-1). In eight animals, the reference stroke volume (ref-SV) was obtained by an electromagnetic flow probe, while reference end-diastolic volume (ref-LVEDV) was computed by dividing ref-SV by undamped thermal dilution ejection fraction (ref-EF) estimates. Comparisons with conductance indexes (z-SV, z-LVEDV and z-EF) were made at baseline, subsequent levels of graded haemorrhage and reinfusion state. In 10 animals intraventricular segmental conductance was compared with echocardiographic left ventricular cross-section (5 MHz short-focus probe), in the basal state and during acute left ventricular volume changes generated by inferior vena cava balloon occlusion. In each experiment, parallel conductance due to the tissues surrounding the left ventricle (Gp) was determined by infusing a 5M NaCl solution bolus into the right ventricle. Linear regression analysis showed fairly good correlations between z-SV, z-LVEDV and z-EF and reference indexes (r = 0.84, r = 0.83, and r = 0.72, respectively; P less than 0.001 in all cases). A linear regression analysis from 17 interventions (inferior vena cava balloon occlusion) showed a good correlation between left ventricular echocardiographic cross-sectional area and conductance, and higher correlation coefficients, r ranging from 0.870 to 0.986 were obtained from continuously sampled conductance and echographic measurements. Parallel conductance Gp was correlated (r = 0.807, P less than 0.01) with the intercept of the regression line of echographic vs conductance data. The determination of Gp thus improved the accuracy of the left ventricular dimension estimate. These results add further evidence for the possibility of continuous monitoring of left ventricular dimension by means of a conductance catheter, and demonstrate the feasibility of such studies on small experimental animals.

[Factors influencing left ventricular function in arterial hypertension]. / Fattori che influenzano la funzione ventricolare sinistra nella ipertensione arteriosa.

Using digitized M-mode echograms we evaluated the role of preload, afterload, inotropic state and left ventricular (LV) mass on LV systolic and diastolic function in 2 groups of hypertensive patients: Group 1: 25 subjects (18 men, mean age 48 +/- 6 years) with normal LV mass (less than 230 g); Group 2: 25 subjects (20 men, mean age 50 +/- 8 years) with LV hypertrophy (wall hypertrophy with normal LV diameter). As control group, we evaluated 50 normal subjects, matched for age, sex and body surface area with hypertensives. LV mass was significantly (p less than 0.001) higher as respect to normals also in hypertensives with normal LV mass; indexes of LV systolic and diastolic function were similar in normals and in hypertensives with normal LV mass and significantly lower in subjects with LV hypertrophy. The end-systolic wall stress was not significantly different in the 2 groups of hypertensives. We evaluated the relative role of preload (end-diastolic LV diameter), afterload (end-systolic wall stress) inotropic state (systolic arterial pressure/end-systolic LV diameter) and LV mass on LV systolic and diastolic function using multiple regression analysis. As regards LV systolic function, the major determinant was the systolic pressure/end-systolic diameter ratio in normals, the end-systolic stress in hypertensives. As regards LV diastolic function, the major determinant was end-systolic stress in normals and hypertensives with normal LV mass, LV mass in hypertensives with myocardial hypertrophy. Preload seems not to influence LV function in normals and in hypertensives with normal LV diastolic diameter. The major determinant of LV systolic function is the inotropic state in normals and the afterload in hypertensives.(ABSTRACT TRUNCATED AT 250 WORDS)

Haemodynamic and neurohormonal responsiveness to different stress tests in mitral valve prolapse.

In this study the blood pressure, heart rate, plasma noradrenaline and plasma adrenaline responses to various forms of sympatho-neural stress were evaluated in patients with mitral valve prolapse (MVP). Sympathetic reactivity in different subgroups of MVP were related to the degree of ventricular arrhythmia. Thirty-eight patients with mitral valve prolapse and 17 healthy controls were studied. All underwent 24-h ECG recording, 2-D echocardiography, head-up tilt to 60 degrees, pressor tests (sustained handgrip, mental arithmetic, cold pressor) and psychological assessment. The blood pressure, noradrenaline and adrenaline response to stress in patients without premature ventricular contraction were similar to those of the controls. In patients with unifocal premature ventricular contraction (PVC) less than 300/h, responses were similar to normal but were associated with higher plasma noradrenaline levels in the basal state and a diminished response to isometric stress. In patients with more than 300/h unifocal premature ventricular contraction, pairs of premature ventricular contraction, or runs of ventricular tachycardia there were lower blood pressure values in the basal state with reduced blood pressure, heart rate and plasma noradrenaline and adrenaline responses to head-up tilt and sustained handgrip, but marked increases in blood pressure, heart rate and plasma noradrenaline levels during the cold pressor test. Our data suggest different degrees of autonomic involvement in mitral valve prolapse which may be related to the various degrees of arrhythmia which seem to contribute to their symptoms.