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Biomedical subjects

G Longobardi

Publications and source records attributed to G Longobardi.

At least 19 recordsLinked to original sources

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

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

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

[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

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

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

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

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

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

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

Left ventricular diastolic filling in elderly hypertensive patients.

OBJECTIVE: To evaluate the effects of mild to moderate hypertension and of LVH on diastolic filling and other Doppler indices in the elderly. DESIGN: Survey with a control group. SUBJECTS: Seventy-one hypertensives (34 men, 37 women) referred for echocardiograms and 32 age- and sex-matched normotensive volunteers. Thirty-six of the hypertensives had LVH; 34 did not. SETTING: Echocardiographic laboratory. MEASUREMENTS: M-mode, two-dimensional, and pulsed Doppler echocardiograms. A wide variety of Doppler-derived indices of diastolic function were assessed. RESULTS: All Doppler derived indices of left ventricular diastolic filling (peak E, peak A, their ratio, EF slope, time-velocity integrals, atrial filling fraction, and isovolumic relaxation time) were similar among the three groups. CONCLUSION: Elderly mild to moderate hypertensives with or without LVH have LV diastolic filling that is normal for age. The identification of pathological diastolic dysfunction requires comparison to age-matched controls, since aging, a major factor influencing diastolic filling, can mask the effect of hypertension.

Age Factors

Effect of beta-adrenoceptor blockade on dipyridamole-induced myocardial asynergies in coronary artery disease.

Twenty-one patients with angiographic evidence of significant coronary artery disease, and positive dipyridamole echocardiographic test results at basal condition and after 7 days of placebo treatment were prospectively studied to see whether beta blockade modifies the effects of dipyridamole echocardiographic testing on regional myocardial contractility. Patients were randomized to propranolol (120 mg/day) or placebo treatment in 3 divided doses for 7 days, after which each patient crossed over to the alternate regimen. Dipyridamole-echocardiographic testing was repeated at the end of each treatment. Propranolol abolished new mechanical signs of transient dipyridamole-induced ischemia (new wall motion abnormalities or an increase in degree of basal asynergies, or both) in 13 of 21 patients. The remaining 8 patients had positive results on dipyridamole echocardiographic testing after the propranolol treatment period. At basal conditions both heart rate and rate-pressure product were significantly reduced with propranolol; there was also a significant decrease in these parameters at peak dipyridamole infusion. At peak dipyridamole infusion heart rate and rate-pressure product were significantly lower in patients with negative than in those with positive echocardiographic test results after propranolol. Our data show that administration of beta blockade significantly reduces the development of transient dipyridamole-induced myocardial asynergies, the earliest markers of acute myocardial ischemia, detected with 2-dimensional echocardiography.

Adrenergic beta-Antagonists

Parental smoking and asthma in childhood.

The effect of parental smoking on childhood asthma was investigated in which data from 302 asthmatic and 433 healthy children aged 1 to 12 years, were studied. All asthmatic patients received prick tests for common allergens. A significantly higher number of heavy parental smokers was found in asthmatic children under 6 years of age with negative prick tests (P = 0.02). A stepwise logistic regression was performed in order to verify interactions between parental smoking and other variables. It is concluded that parental smoking is an important risk factor for "prick test negative" asthmatic children aged 6 years or less.

Asthma

Regional left ventricular mechanical function during isometric exercise in patients with coronary artery disease: correlation with regional coronary blood flow changes.

The effects of isometric exercise on regional left ventricular mechanical function and regional coronary blood flow were evaluated in 17 patients with significant proximal stenosis of the left anterior descending coronary artery and 10 patients with normal coronary arteriograms. All patients had normal myocardial contractility in the basal condition. All performed isometric handgrip exercise at 50% of the maximal voluntary contraction for 3 min during two-dimensional echocardiographic monitoring and hemodynamic evaluation of great cardiac vein flow by thermodilution technique. During isometric exercise, 7 of the 17 patients with left anterior descending coronary stenosis developed asynergy in the anterior territory (anterior or septal segment, or both) (group I); the remaining 10 showed normal myocardial contraction during the test (group II). The 10 normal subjects manifested no regional asynergy during the test (control group). The increase in great cardiac vein flow at peak isometric exercise was significantly smaller (p less than 0.01) in group I (+15 +/- 8%) than that in group II (+98 +/- 48%) and the control group (+64 +/- 22%). Anterior coronary vascular resistance decreased in group II (-32 +/- 13%) and in the control group (-25 +/- 8%) but increased in group I (+6 +/- 8%, p less than 0.01 versus group II and control group). These data demonstrate that handgrip-induced myocardial asynergy is associated, in our study patients, with an abnormal response of the regional coronary circulation. The increase in coronary vascular resistance in group I patients with asynergy demonstrates that functional mechanisms play a dominant role in left ventricular mechanical dysfunction induced by isometric exercise.

Aged

[Action of magnesium salts on the toxic effects of calcium overload in the isolated and perfused rat heart].

The toxic effect of calcium overload and the action of magnesium sulfate (4 mM) and magnesium chloride (4 mM) on heart rate, coronary flow rate, left ventricular systolic pressure, dp/dt max and voltage epicardial electrogram were studied in the isolated and perfused rat heart. Increasing calcium load by increasing [Ca]o from 1 to 6 mM we observed a progressive increase in heart rate coronary flow rate, left ventricular systolic pressure, dp/dt max and a decrease in voltage epicardial electrogram. During the exposure to [Ca]o 8 mM the toxic manifestations of calcium overload developed and we observed a reduction in heart rate, coronary flow rate, left ventricular systolic pressure, dp/dt max and an increase in voltage epicardial electrogram. Magnesium sulfate and magnesium chloride had similar effect: in fact, in both procedures we observed a decrease in heart rate, left ventricular systolic pressure, dp/dt max, voltage epicardial electrogram and an increase in coronary flow rate at [Ca]o 2 mM. When magnesium salts were administered at the same time as the heart was exposed to [Ca]o 8 mM, we observed a reduction in the toxic effect of calcium overload. When magnesium salts were administered after the appearance of the calcium overload, they did not revert the toxic effect of calcium overload but prevented the insurgence of cardiac standstill. Thus, in the isolated perfused rat heart, the toxic manifestations of calcium overload develop at [Ca]o 8 mM and magnesium salts are able to reduce the toxic effects of calcium overload and the appearance of cardiac standstill according to their calcium-antagonism mechanism.

Animals