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Biomedical subjects

G Longobardi

Publications and source records attributed to G Longobardi.

At least 19 recordsLinked to original sources
PubMed2001

High level of physical activity preserves the cardioprotective effect of preinfarction angina in elderly patients.

OBJECTIVES: The study investigated the effects of physical activity on preinfarction angina, a clinical equivalent of ischemic preconditioning (PC), in adult and elderly patients with acute myocardial infarction (AMI). BACKGROUND: Preinfarction angina seems to confer protection against in-hospital mortality in adult but not in elderly patients. However, it has been experimentally demonstrated that exercise training restores the protective effect of PC in the aging heart. METHODS: We retrospectively verified whether physical activity preserved the protective effect of preinfarction angina against in-hospital mortality in 557 elderly patients with AMI. Physical activity was quantified according to the Physical Activity Scale for the Elderly (PASE). RESULTS: In-hospital mortality was 22.2% in elderly patients with preinfarction angina and 27.2% in those without (p = 0.20). When the PASE score was stratified in quartiles (0 to 40, 41 to 56, 57 to 90, >90), a high score was strongly associated with reduced in-hospital mortality (30.8%, 32.2%, 17.2% and 15.3%, respectively, p < 0.001 for trend). Interestingly, a high level of physical activity reduced in-hospital mortality in elderly patients with preinfarction angina (35.7%, 35.4%, 12.3% and 4.23%, respectively, p < 0.001 for trend) but not in those without (23.0%, 27.2%, 26.0% and 35.0%, respectively, p = 0.35 for trend). Accordingly, the protective role of preinfarction angina on in-hospital mortality was present only in elderly patients showing a high level of physical activity (adjusted odds ratio, 0.09; 95% confidence interval, 0.01 to 0.57; p < 0.05). CONCLUSIONS: Physical activity and not preinfarction angina protects against in-hospital mortality in elderly patients with myocardial infarction. Nevertheless, the protective effect of preinfarction angina is preserved in elderly patients with a high level of physical activity.

Age Distribution↗
PubMed2000

Exercise training restores ischemic preconditioning in the aging heart.

OBJECTIVES: To investigate the effects of ischemic preconditioning in hearts from adult and both sedentary and trained senescent rats. BACKGROUND: Ischemic preconditioning does not prevent postischemic dysfunction in the aging heart, probably because of reduction of cardiac norepinephrine release. Exercise training can reverse the age-related decrease of norepinephrine production. METHODS: We investigated the effects on mechanical parameters of ischemic preconditioning against 20 min of global ischemia followed by 40 min of reperfusion in isolated perfused hearts from adult (six months) and sedentary or trained (six weeks of graduated swim training) senescent (24 months) rats. Norepinephrine release in coronary effluent was determined by high-performance liquid chromatography. RESULTS: Final recovery of percent-developed pressure was significantly improved after preconditioning in adult hearts (91.6+/-9.6%) versus unconditioned controls (54.2+/-5.1%, p<0.01). The effect of preconditioning on developed pressure recovery was absent in sedentary but present in trained senescent hearts (39.6+/-4.1% vs. 64.3+/-7.1%, p<0.05). Norepinephrine release significantly increased after preconditioning in adult and in trained but not in sedentary senescent hearts. The depletion of myocardial norepinephrine stores by reserpine abolished preconditioning effects in adult and trained senescent hearts. CONCLUSIONS: In adult and trained but not in sedentary senescent hearts, preconditioning reduces postischemic dysfunction and is associated with an increase in norepinephrine release. Preconditioning was blocked by reserpine in both adult and trained senescent hearts. Thus, exercise training may restore preconditioning in the senescent heart through an increase of norepinephrine release.

Aging↗
PubMed2000

"Warm-up" phenomenon in adult and elderly patients with coronary artery disease: further evidence of the loss of "ischemic preconditioning" in the aging heart.

BACKGROUND: A reduction of exercise-induced ischemia in patients with coronary artery disease by means of brief period of exercise followed by resting is called the "warm-up" phenomenon. This phenomenon may represent a clinical counterpart of "ischemic preconditioning." We studied the warm-up phenomenon in both adult and elderly patients with similar angiographic evidence of coronary artery disease, using three exercise tests after excluding the "training effect." METHODS: In order to verify the presence of "training effect," three exercise tests were performed in days 1, 2, and 3 ("training" tests). The third test was used as baseline for a successive test, performed after a recovery period of 10 minutes to reestablish baseline electrocardiographic conditions. A third exercise test was performed 30 minutes later ("warm-up" tests). RESULTS: "Training" tests did not differ in all parameters in both adult and elderly patients. "Warm-up" tests showed that time to onset 1-mm ST depression was significantly higher (p < .001). whereas ST depression and time to recovery was significantly lower in the second and third test in adult but not in elderly patients (p < .001 ). Difference (in seconds) in the time at which 1-mm ST depression occurred on first warm-up exercise compared with the second was inversely correlated with age (p < .001 ). CONCLUSIONS: Previous exercise followed by resting is able to reduce the successive exercise-induced ischemia ("warm-up" phenomenon) in adult but not in elderly patients with coronary artery disease. This is independent of a greater age-related severity of coronary disease and of "training effect." These results confirm the hypothetical age-related reduction of "ischemic preconditioning" in aging heart.

Adaptation, Physiological↗
PubMed2000

Echo-dipyridamole stress test evaluation of isosorbide-5-mononitrate efficacy and tolerance in patients with coronary heart disease: interplay with sympathetic activity.

In 22 patients with stable myocardial ischemia, we prospectively studied the short- and long-term effects of isosorbide-5-mononitrate (5-ISMN) on dipyridamole-induced myocardial ischemia, the ability of dipyridamole-stress echocardiography to evaluate nitrate tolerance, and the role of activation of the neurohumoral system in nitrate tolerance development, assessed by modifications of catecholamines plasma levels and heart rate variability. After brief treatment with 5-ISMN, dipyridamole-stress echocardiography was negative in 19 of 22 patients (p < 0.001 vs. placebo). During the sustained phase, dipyridamole-stress echocardiography was positive after both placebo and active drug (p = NS vs. placebo). Heart rate variability showed significantly higher values in power of the low frequency (LF) band and low- to high-frequency ratio (L/H), as well as significantly lower values of the power of the high-frequency (HF) band (all p < 0.001) during brief but not during sustained administration of 5-ISMN. Norepinephrine plasma levels were significantly higher (p < 0.001) during short-term 5-ISMN administration but not during the sustained phase. Our results indicate that short-term administration of 5-ISMN antagonizes dipyridamole-induced myocardial ischemia and show the loss of antiischemic efficacy in 95% of patients during sustained treatment, demonstrating that dipyridamole-stress echocardiography is a useful tool to assess the presence of nitrate tolerance. Spectral analysis of heart rate variability and norepinephrine values confirm that brief nitrate administration increases sympathetic activity, a possible crucial trigger event in the development of nitrate tolerance, whereas prolonged nitrate treatment is not associated with prolonged neurohumoral activation.

Aged↗
PubMed1999

Intracoronary serotonin release after high-pressure coronary stenting.

It is known that platelet-derived serotonin at the site of coronary angioplasty induces an increase in coronary tone and plays a role in vasoconstriction after balloon angioplasty. The goal of the present investigation was to compare local release of serotonin with changes in coronary tone after coronary stenting and coronary angioplasty. Twenty patients with significant stenosis (> or =50% diameter narrowing) of the left anterior descending coronary artery were referred to traditional coronary angioplasty (10 patients; group 1) or high-pressure coronary stenting (10 patients; group 2). An additional 16 patients with similar angiographic characteristics were referred to the coronary angioplasty group (8 patients; group 1a) or stenting group (8 patients; group 2a) after pretreatment with ketanserin. Serotonin plasma levels in coronary sinus and coronary cross-sectional area distal to the site of dilatation were measured before and after bath revascularization procedures. In groups 1 and 1a, plasma serotonin levels in coronary sinus increased from basal values of 3.2+/-0.8 and 3.2+/-0.5 ng/ml to 29.5+/-13 and 25.6+/-9 ng/ml after ballooning (p <0.001 vs baseline). In groups 2 and 2a, plasma serotonin levels in coronary sinus increased from basal values of 3.5+/-0.3 and 3.5+/-0.7 ng/ml to 114.6+/-34 and 113+/-29 ng/ml after stenting (p <0.001 vs baseline and vs postangioplasty values in groups 1 and 1a). Coronary cross-sectional area distal to the site of dilatation significantly decreased after angioplasty in group 1 (from 4.33+/-0.4 to 3.32+/-0.3 mm2; p <0.001), and after stenting in group 2 (from 4.27+/-0.3 to 2.86+/-0.2 mm2; p <0.001 vs baseline, and p <0.02 vs values after coronary angioplasty in group 1). Pretreatment with ketanserin significantly reduced distal coronary vasoconstriction after angioplasty and stenting. It is concluded that the higher local serotonin release after coronary stenting may explain the more marked coronary constriction observed after prosthesis deployment with respect to traditional coronary angioplasty. Ketanserin is able to significantly attenuate the increase in distal coronary tone induced by both revascularization procedures.

Angioplasty, Balloon, Coronary↗
PubMed1999

Verapamil reduces dipyridamole-induced myocardial ischemia in patients with coronary artery disease.

The aim of this study was to evaluate the effects of verapamil administration on dipyridamole-induced transient wall-motion abnormalities as detected by two-dimensional echocardiographic monitoring in patients with coronary artery disease. Twenty-eight patients (16 men and 12 women; mean age, 60+/-7 years) with angiographic evidence of significant coronary artery disease, positive dipyridamole echocardiography test results at basal condition on two consecutive days, were prospectively studied. Patients were randomized to verapamil (360 mg/day) or placebo treatments, given in three divided doses daily for 7 days; at the end of this time, each patient crossed over to the alternate regimen. Dipyridamole echocardiographic testing was repeated at the end of each treatment period. Our data demonstrate that verapamil significantly reduces the dipyridamole-induced wall-motion score index, a quantitative marker of acute myocardial ischemia (1.7+/-0.4 vs. 1.3+/-0.2; p<0.001). Hemodynamic data show that the drug reduces heart rate and rate-pressure product at basal condition (heart rate from 75+/-8 to 67+/-9 beats/min; p<0.001; rate-pressure product from 99+/-13 to 86+/-13 U x 10(-2); p<0.001) and at peak dipyridamole infusion (heart rate from 96+/-8 to 89+/-6 beats/min; p<0.001; rate pressure product from 127+/-21 to 118+/-13 U x 10(-2); p<0.05) with respect to placebo treatment. We conclude that verapamil is able to reduce dipyridamole-induced ischemia, as detected by two-dimensional echocardiographic monitoring, in patients with coronary artery disease by reducing, at least partially, myocardial oxygen consumption. Moreover, its beneficial action could be related to the effects of the drug on coronary collateral circulation and on sympathetic modulation.

Aged↗
PubMed1997

Angina-induced protection against myocardial infarction in adult and elderly patients: a loss of preconditioning mechanism in the aging heart?

OBJECTIVES: The present study examined whether angina 48 h before myocardial infarction provides protection in adult and elderly patients. BACKGROUND: The mortality rate for coronary artery disease is greater in elderly than in young patients. In experimental studies, ischemic preconditioning affords an endogenous form of protection against ischemia-reperfusion injury in adult but not in senescent hearts. Angina before myocardial infarction, a clinical equivalent of experimental ischemic preconditioning, has a protective effect in adult patients. It is not known whether angina before myocardial infarction is also protective in aged patients. METHODS: We retrospectively verified whether antecedent angina within 48 h of myocardial infarction exerts a beneficial effect on in-hospital outcomes in adult (< 65 years old, n = 293) and elderly (> or = 65 years old, n = 210) patients. RESULTS: In-hospital death was more frequent in adult patients without than in those with previous angina (10% vs. 2.6%, p < 0.01), as were congestive heart failure or shock (10.7% vs. 3.3%, p < 0.02) and the combined end points (in-hospital death and congestive heart failure or shock) (20.7% vs. 5.9%, p < 0.0003). In contrast, the presence or absence of previous angina before acute myocardial infarction in elderly patients seems not to influence the incidence of in-hospital death (14.4% vs. 15.2%, p = 0.97), congestive heart failure or shock (11.0% vs. 11.9%, p = 0.99) and the combined end points (25.4% vs. 27.1%, p = 0.89). Logistic regression analysis models for in-hospital end points show that previous angina is a positive predictor in adult but not in elderly patients. CONCLUSIONS: The presence of angina before acute myocardial infarction seems to confer protection against in-hospital outcomes in adults; this effect seemed to be less obvious in elderly patients. This study suggests that the protection afforded by angina in adult patients may involve the occurrence of ischemic preconditioning, which seems to be lost in senescent patients.

Adult↗
PubMed1996

Preconditioning does not prevent postischemic dysfunction in aging heart.

OBJECTIVES: This study was performed to investigate the effect of single or multiple brief periods of ischemia and the administration of exogenous norepinephrine before a more prolonged ischemic period and after reperfusion in adult and senescent isolated and perfused rat hearts. BACKGROUND: The mortality rate for coronary artery disease is greater in the elderly. Ischemic preconditioning has been proposed as an endogenous form of protection against ischemia-reperfusion injury. However, the role of preconditioning in aging heart is unknown. METHODS: We compared the protective effect of preconditioning transient ischemic and norepinephrine stimuli against 20 min of global normothermic ischemia and 40 min of reperfusion in isolated perfused hearts of adult (6 months old) and senescent (24 months old) rats. Norepinephrine release in coronary effluent was determined by high performance liquid chromatography. RESULTS: Final recovery of percent developed pressure was improved after single preconditioning transient ischemic and norepinephrine stimuli in adult hearts (87.7 +/- 9% and 82.3 +/- 8.7%) versus unconditioned control hearts (50.6 +/- 4.8%, p < 0.01 [mean +/-SD]). The effect of preconditioning on developed pressure recovery was not present in senescent hearts after transient ischemic stimulus (39.8 +/- 4.9% vs. 41.6 +/- 5.8%, p = NS) but was present after norepinephrine stimulus (74.3 +/- 10.5, p < 0.01). Norepinephrine release significantly increased after preconditioning transient ischemic stimulus in adult but not in senescent hearts (p < 0.01 vs. adult). Transient ischemic- and norepinephrine-induced preconditioning was blocked by alpha-adrenergic receptor antagonists in both adult and senescent hearts. Multiple transient ischemic stimuli were able to reduce postischemic dysfunction in adult but not in senescent hearts. CONCLUSIONS: Preconditioning transient ischemic stimulus significantly reduces postischemic dysfunction in adult but not in senescent hearts, whereas exogenous norepinephrine is able to mimic preconditioning in both adult and senescent hearts. Ischemic preconditioning induces an increase in norepinephrine release in adult but not in senescent hearts. Preconditioning induced by transient ischemic stimulus and norepinephrine was abolished by alpha-adrenergic receptor blockade in both adult and senescent hearts. Thus, our data demonstrate that preconditioning is absent in aging heart and is probably related to the reduction of norepinephrine release and alpha-adrenergic receptor stimulation in response to ischemic preconditioning.

Aging↗
PubMed1996

Effects of age on the role of atrial natriuretic factor in renal adaptation to physiologic variations of dietary salt intake.

The effects of normal, low, and high dietary salt intake on basal atrial natriuretic factor plasma levels, plasma renin activity, and aldosterone were evaluated in seven young (Group 1), seven middle-aged (Group 2), and seven elderly healthy volunteers (Group 3). In all subjects, progressively higher doses of human alpha-atrial natriuretic factor were infused at low-sodium diet conditions to obtain hormone plasma values during infusion similar to those obtained in the same subjects at high-sodium diet conditions. Atrial natriuretic factor plasma values were significantly higher in Group 3 than in the other two groups at both normal- and high-salt diet conditions, and at all steps of the infusion study. At low-sodium diet conditions, peptide concentrations averaged 23.2 +/- 6.2 in Group 3, 26.2 +/- 1.9 in Group 2, and 19.1 +/- 3.9 pg/mL in Group 1 (P = not significant between groups). Hormone plasma values at high-salt diet conditions averaged 47 +/- 6.9 pg/mL in Group 1, 60 +/- 6.5 pg/mL in Group 2, and 136.3 +/- 14.6 pg/mL in Group 3. Each value was not significantly different from the corresponding value gained at an infusion step of 2 ng/min per kg in Group 1 and 2 (57.1 +/- 11.9 and 62.7 +/- 6.5 pg/mL, respectively), and of 1 ng/min per kg (139.1 +/- 22.2 pg/mL) in Group 3. At these infusion steps and at high-salt diet conditions, the urinary sodium excretion rate was, respectively, 0.185 +/- 0.02 and 0.311 +/- 0.02 mEq/min in Group 1, 0.168 +/- 0.01 and 0.300 +/- 0.02 mEq/min in Group 2, and 0.110 +/- 0.01 and 0.256 +/- 0.01 mEq/min in Group 3. Hormone infusion induced a progressive fall of plasma renin activity and aldosterone level in all groups. By experimentally increasing plasma concentrations of atrial natriuretic factor in a low-salt diet condition to the levels occurring physiologically in a high-salt diet condition, a significant rise in urinary sodium excretion rate is evoked, which accounts for 52% in young, 47% in middle-aged, and 30% in older subjects of the rise that is necessary to balance the increased salt intake.

Adaptation, Physiological↗
PubMed1996

[The functional therapy of fractures of the mandibular condyle. Our experience].

This work dealt with clinical experience since 1992, in management by functional therapy of mandibular condyle fractures, of the Institute of Oral and Maxillo-Facial Surgery in the I Policlinico of Naples. In this work from 87 treated patients, only a group of 8 has been considered because it expresses the heterogeneity of all cases about the age, the sex, the kind and the level of fracture and the association with other fracture of the skull. The results obtained show that the functional therapy must be considered the first opinion in the mandibular condylar fractures at least there are specific conditions.

Adolescent↗
PubMed1995

Failure of protective effect of captopril and enalapril on exercise and dipyridamole-induced myocardial ischemia.

Fifteen patients with angiographic evidence of significant coronary artery disease, exertional myocardial ischemia, and positive dipyridamole echocardiographic test results at basal conditions and after 7 days of placebo treatment were prospectively studied to see whether captopril (containing sulfhydryl) and enalapril (nonsulfhydryl) modify myocardial ischemia induced by exercise testing and the effects of dipyridamole echocardiographic testing on regional myocardial contractility. Patients were randomized to captopril (150 mg/day in 3 separate doses) or enalapril (20 mg/day) for 1 week. At the end of this period each patient crossed over to the alternate regimen after a washout period of 7 days. Exercise stress testing and dipyridamole echocardiographic testing were repeated at the end of each treatment period. Neither captopril nor enalapril had a significantly greater anti-ischemic effect than placebo in any patient. Exercise duration, time to onset of ST-segment depression, maximal workload, degree of ST-segment depression, and rate-pressure product were not affected by either drug. Neither captopril nor enalapril improved dipyridamole-induced mechanical dysfunction or ST-segment depression.

Adult↗
PubMed1995

Congestive heart failure in elderly patients: controlled study of delapril versus captopril.

In this controlled trial, 30 elderly patients with congestive heart failure, New York Heart Association (NYHA) classes II and III, were randomly assigned to treatment with captopril 25 mg three times daily or delapril 15 mg twice daily. At the end of an 8-week treatment period, clinical symptoms of heart failure were significantly relieved by both drugs, with a consistent and statistically significant improvement in patients' quality of life evaluated using a symptoms/activity scale (p < 0.001). None of the patients was judged NYHA class III at the end of the trial and 40% were assigned to class I (p < 0.01). There was a relevant, but not statistically significant, increase in exercise duration in both treatment groups (10% captopril group, 14% delapril group), but the number of patients discontinuing the exercise test for dyspnea was 50% less in the delapril group. Neither drug had evident effects on echocardiographic left ventricular parameters. Two patients treated with captopril and 3 with delapril complained of mild-to-moderate adverse reactions. The safety of both drugs was confirmed by laboratory tests.

Aged↗
PubMed1995

Age-response effectiveness of gallopamil for the treatment of myocardial exertional ischemia. A medium-term randomized cross-over double-blind placebo-controlled trial.

We evaluated the efficacy and safety of gallopamil 150 mg daily in middle-aged and elderly patients with stable exertional ischemia, using a medium-term randomized double-blind cross-over placebo-controlled trial. Twenty middle-aged patients (52.8 +/- 6 years; range 38-61 years) and 14 elderly patients (67.4 +/- 2.8 years; range 65-73 years) with stable exertional ischemia underwent a bicycle exercise test. After a run-in period, both groups received treatment with either placebo or gallopamil 50 mg tid for 28 days. At the end of this time, each patient crossed over to the alternate regimen. Gallopamil significantly reduced heart rate, blood pressure and rate pressure product (from 15.37 +/- 2.7 to 13.65 +/- 4.16 U x 10(-3); p < 0.01) in elderly patients at submaximal exercise, but had no effect in middle-aged patients (from 14.52 +/- 4.45 to 13.49 +/- 3.77 U x 10(-3); p = NS). At peak exercise, none of the hemodynamic parameters was modified with gallopamil in either group. At peak exercise, both middle-aged and elderly patients achieved rate-pressure products similar to those reached during placebo at higher work loads. Exercise duration and maximal work load significantly increased in both groups. Electrocardiographic signs of ischemia were favorably influenced by gallopamil in both groups (from 1.39 +/- 0.5 mm to 0.76 +/- 0.73 mm; p < 0.001 in the middle-aged patients and from 1.5 +/- 0.34 mm to 1 +/- 0.76 mm; p < 0.01 in the elderly patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Left ventricular diastolic filling in diabetes mellitus with and without hypertension.

Left ventricular diastolic filling by Doppler echocardiography was investigated in 84 diabetic patients without evidence of heart disease and in 84 normotensive nondiabetic age- and sex-matched control subjects. Diabetic patients were subdivided into two groups on the basis of the presence of arterial hypertension. Group 1 comprised 41 normotensive diabetic patients (19 men, 22 women, mean age 63.7 +/- 9.1 years); Group 2 comprised 43 hypertensive diabetics (15 men, 28 women, mean age 65.6 +/- 9.6 years). Doppler measures of diastolic filling were significantly altered in the two groups as compared with control subjects. Peak atrial flow velocity, velocity integral for the atrial filling period, and atrial filling fraction were increased, whereas the ratio of peak early to peak atrial flow velocity and the ratio of flow velocity integrals were decreased, especially in Group 2 patients. Thirteen patients in Group 1 (32%) and 17 in Group 2 (40%) had evidence of diastolic dysfunction, as assessed by the presence of at least two independent abnormal indices (outside age-corrected 95% confidence interval). In each group, patients with altered diastolic filling differed slightly from diabetic patients with normal Doppler indices, tending to increased wall thickness and left ventricular mass. In conclusion, diastolic filling of the left ventricle is frequently altered in diabetic patients and is adversely affected by arterial hypertension whose coexistence further impairs left ventricular relaxation.

Aged↗
PubMed1995

Protective effect of beta-blockade on dipyridamole-induced myocardial ischaemia. Role of heart rate.

This study was designed to investigate the effect of heart rate changes on dipyridamole echocardiographic tests in patients with coronary artery disease treated with propranolol. We prospectively studied 12 patients (8 men and 4 women; mean age 56.5 +/- 8.7 years) selected by: (a) angiographic evidence of significant coronary artery disease; (b) adequate echocardiographic window; (c) positive dipyridamole echocardiography test results in baseline conditions (step I); (d) test reproducibility in the absence of treatment; (e) negative dipyridamole echocardiography test results after 7 days of treatment with propranolol (120 mg.day-1) in twice divided doses daily (step II). In all patients treated with propranolol, dipyridamole echocardiographic testing was repeated 24 h after the last negative test. In these patients, transoesophageal atrial pacing was performed at peak dipyridamole infusion to increase heart rate to values similar to those observed at baseline (step III). At baseline, heart rate and rate-pressure product were significantly lower in patients treated with propranolol (-20.3% and -22.5% in group II, P < 0.001 vs step I; -24.3% and -26.4% in group III, P < 0.05 vs step I), but the different treatments did not produce significant differences in systolic and diastolic blood pressure. At peak dipyridamole infusion, heart rate and rate-pressure product increased with either placebo or propranolol treatments with respect to baseline, while remaining significantly lower with propranolol as compared to placebo (-29.6% and -29.5% in step II, P < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1995

Relation between age, left ventricular mass and ventricular arrhythmias in patients with hypertension.

To evaluate the effect of age on left ventricular hypertrophy-related arrhythmias in patients with essential arterial hypertension, 68 hypertensives (47 men and 21 women, mean age 59.4 +/- 9.5 years) without other cardiovascular disorders were studied. All patients underwent M-mode and two-dimensional echocardiogram and 24 h ambulatory electrocardiographic monitoring to measure left ventricular internal dimension, septum and posterior wall thickness, left ventricular mass index, premature ventricular beats and modified Lown grade. Premature ventricular beats (PVB) and modified Lown grade were significantly related to left ventricular mass index, but not to left ventricular internal dimension, fractional shortening, systolic and diastolic blood pressure. There was no relation between age and number of PVB, or severity of arrhythmias. In conclusion, in hypertensive patients only left ventricular hypertrophy, and not age, plays a significant role in the pathophysiology of the increased incidence of ventricular arrhythmias by a different mechanism than age-related increased ventricular arrhythmias.

Adult↗