PubMed Health⌕ Search

Biomedical subjects

P I Altieri

Publications and source records attributed to P I Altieri.

At least 19 recordsLinked to original sources
PubMed2001

[Total plasma homocysteine concentrations in Puerto Rican patients with ischemic heart disease].

INTRODUCTION AND OBJECTIVES: In Puerto Rico, it has been established that although coronary disease is the leading cause of death, the population has a lower incidence of coronary disease than in the continental United States. In addition, the severity of the disease is less aggressive in terms of a lower incidence of ventricular tachycardia and sudden death. One factor that could contribute to the lower incidence of coronary disease in Puerto Rico is that our population might have lower total plasma homocysteine concentrations (tHcys) than in the continental United States. Our main objective was to measure tHCys in the Puerto Rican population with atherosclerotic cardiovascular disease (ACD). METHODS: We randomly measured tHcys concentrations in seventy Puerto Rican patients who were hospitalized at the Cardiovascular Center of Puerto Rico and the Caribbean (UPR Division). RESULTS: The mean tHCys concentration in these patients is similar to those reported for the Framingham study when adjusted by age (11.2 vs. 11.8 micromol/l). In the Puerto Rican population, males had a higher tHcys concentration than females (11.7 vs 9.5 micromol/l, p = 0.07). In addition, we did not see an increase of tHcys concentrations in diabetic patients when compared with non-diabetics (10.1 vs. 11.2 micromol/l, p = 0.74). We did not see a direct correlation between tHcys concentrations and heart condition as measured by coronary angiography (normal = 11.1 micromol/l, light = 10.5 micromol/l, moderate = 10.9 micromol/l, severe = 10.5 micromol/l; Kruskal-Wallis = 0.45) either. CONCLUSION: These results suggest that tHcys concentration is not a good predictor of the seriousness of ACD in the Puerto Rican patient population.

Female↗
PubMed2000

Relationship between NO synthesis, arginine transport, and intracellular arginine levels in vascular smooth muscle cells.

The present study was designed to evaluate the relevance of arginine transport in nitric oxide (NO) synthesis in vascular smooth muscle cells. For this purpose, NO synthesis and arginine transport (system B0,+ and y+) were evaluated in cells treated with IL-1beta or angiotensin II (Ang II). In addition, the effects of 5 mM lysine and glutamine, competitive inhibitors of systems y+ and B0,+ respectively, were examined. L-arginine transport was estimated with 3H-labelled arginine and NO was determined with the Griess reagent. These studies were done in control conditions, arginine-starved cells, and in cells incubated in media containing 10 mM arginine. Our data indicate that induction of NO biosynthesis by IL-1beta depends on external arginine when cells are arginine-depleted for 24 hours. The concentration of arginine producing half maximal activation of NO synthesis in arginine-depleted cells ([arginine]i < 10 microM) was 41.1 +/- 18 microM. By contrast, in normal culture conditions, NO synthesis occurred independently of arginine transport. Neither 5 mM lysine or glutamine which abolished arginine transport through systems y+ and B0,+, respectively, reduced nitrite release in cells incubated in normal media. This suggests that the relevance of arginine uptake to NO synthesis depends on the status of intracellular arginine pools. Intracellular arginine concentrations were not affected by the stimulation of NO production using IL-1beta or its inhibition using Ang II, but were markedly reduced by arginine starvation for 48h. Aspartate levels were also reduced by arginine-depletion, but were not affected in cells incubated with 10 mM arginine. By contrast, glutamate levels were reduced in arginine-starved cells and were increased in cells incubated in arginine-supplemented medium. Ornithine levels were markedly increased by arginine supplementation. Altogether, these findings indicate that NO synthesis is normally independent of membrane transport. However in arginine-depleted cells, membrane transport is essential for NO synthesis. It is concluded that arginine transport is required for the long-term maintenance of intracellular arginine pools.

Angiotensin II↗
PubMed2000

Total plasma homocysteine concentrations in Puerto Rican patients with presumptive atherosclerotic coronary disease.

BACKGROUND: In Puerto Rico, it has been established that although coronary heart disease is the leading cause of death, the population has a lower incidence of coronary disease than the continental United States. In addition, the severity of the disease is less aggressive in terms of a lower incidence of ventricular tachycardia and sudden death. A factor in the lower incidence of coronary disease in Puerto Rico could be a lower total plasma homocysteine concentration (tHcys) in our population. METHODS: We randomly measured tHcys concentrations in seventy-two Hispanic patients who were hospitalized for coronary angiography at the Cardiovascular Center of Puerto Rico and the Caribbean (UPR Division). RESULTS: The mean tHCys concentration in our patient population is similar than that reported for the Framingham study when adjusted by age (11.2 mumol/L vs. 11.8 mumol/L). In the Puerto Rican population, males had a higher tHcys concentration than females but this difference was not statistically significant (10.9 mumol/L vs. 9.4 mumol/L, p = 0.09). In addition, we did not see an increase of tHcys concentrations in diabetic patients when compared with nondiabetics (10.1 mumol/L vs. 10.3 mumol/L, p = 0.73). Neither we saw a direct correlation between tHcys concentrations and atherosclerosis as measured by coronary angiography (normal = 10.9 mumol/L, mild = 8.6 mumol/L, moderate = 10.9 mumol/L, severe = 10.5 mumol/L; ANOVA = 0.29). CONCLUSIONS: These results suggest that tHcys concentration is not a good predictor of atherosclerotic coronary disease in our patient population.

Angiography↗
PubMed1997

Altered vascular function in early stages of heart failure in hamsters.

BACKGROUND: Congestive heart failure is a clinical condition associated with alterations in the normal balance of neurohumoral agents and factors acting on the vascular wall. The etiology of this condition, however, remains largely undefined. To help elucidate the pathophysiology of this disease, vascular function and angiotensin-converting enzyme activity were evaluated in 2-month-old Syrian cardiomyopathic hamsters (SCHs) that had not yet developed heart failure. Age-matched normal hamsters were used as control hamsters. METHODS AND RESULTS: Vascular function studies included determinations of contractile responses of aortic rings to 0.1 microM angiotensin II and 0.1 microM norepinephrine. In addition, endothelial function was evaluated by the vasorelaxant action of acetylcholine on norepinephrine-precontracted aortic rings. The results indicate that the pressor effect of angiotensin II (0.1 microM) was 35% greater in aortic rings from SCRs than that observed in control animals. This effect is specific for angiotensin II because the contraction induced by NE (0.1 microM) was similar in both of these strains. Angiotensin-converting enzyme activity was three-fold higher in aorta homogenates from SCHs but normal in plasma and heart tissue when compared with control hamsters. Aortic ring preparations from SCHs also exhibited endothelial dysfunction because the maximal relaxation elicited by 10 microM acetylcholine was reduced 53%. Concentration-response curves with acetylcholine yielded EC50 values that were threefold lower in SCHs (97.2 +/- 0.1 nM) than in control animals (286 +/- 7 nM). Indomethacin (1 microM) increased the vasorelaxant effect of acetylcholine 28% in SCHs and shifted to the left the concentration-response curve of this agonist, suggesting an increased relaxation with the cyclooxygenase inhibitor. No effect of indomethacin on acetylcholine-induced relaxation was observed in control animals. Sodium nitroprusside induced similar relaxations in both control animals and SCHs, suggesting that the vascular smooth muscle response is normal in SCR. CONCLUSIONS: Altogether these results point to a state of enhanced vascular contractility in young SCHs that could predispose these animals to develop heart failure, the enhanced vascular contractility could result from increased activity of the local renin-angiotensin system, augmented vascular response to angiotensin II, reduced nitric oxide synthesis, and enhanced production of prostaglandins.

Animals↗
PubMed1996

Simvastatin releases Ca2+ from a thapsigargin-sensitive pool and inhibits InsP3-dependent Ca2+ mobilization in vascular smooth muscle cells.

Simvastatin (SV), an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity inhibits migration and proliferation of vascular smooth muscle cells (SMC). To investigate whether these effects of SV are related to inhibition of cell calcium mobilization, cultured SMC obtained from rat aorta were loaded with Fura-2 to determine the basal cytosolic free calcium levels ([Ca2+]i) and the agonist-stimulated Ca2+ mobilization. SV (20 mu M) transiently increased cytosolic free calcium, an effect that depends mainly on intracellular calcium release (68%). This effect of SV was markedly reduced (75%) by thapsigargin, an inhibitor of the Ca2+ ATPase of inositol 1,4,5-triphosphate (InsP3)-sensitive calcium pools. Incubation of cells with SV (15 min) inhibited the mobilization of Ca2+ by angiotensin II, platelet-derived growth factor, and vasopressin (IC50 = 5 mu M). SV did not affect inositol trisphosphate (InsP3) levels or modify its generation by angiotensin II (Ang II) and vasopressin. Furthermore, in saponin-permeabilized cells, SV abolished the release of calcium by 2,3-dideoxy-InsP3. SV reduced the effect of thapsigargin on InsP3-sensitive stores by 67%, suggesting that SV depletes these calcium pools. The inhibitory effect of SV on calcium mobilization was prevented by coincubation of cultured cells (24 h) with 1 mM mevalonic acid, the product of HMG-CoA reductase activity. These results support the notion that SV inhibits [corrected] the migration and proliferation of SMC by directly affecting cell Ca2+.

Angiotensin II↗
PubMed1996

Inhibition of smooth muscle cell calcium mobilization and aortic ring contraction by lactone vastatins.

OBJECTIVE: To determine the effects of vastatins on the contraction of rat aortic rings and to assess their effects on calcium mobilization using cultured smooth muscle cells from rat aorta. METHODS: Aortic rings from Sprague-Dawley rats were mounted on stainless steel wires to determine the generation of tension using force-displacement transducers. The tension (g) developed by angiotensin II (100 nmol/l) was measured under basal conditions and after 45 min incubation with 20 micromol/l simvastatin. The effect of 20 mol/l simvastatin, lovastatin, mevastatin and pravastatin on noradrenaline concentration-response curves and the angiotensin II-induced calcium mobilization was also evaluated. RESULTS: Addition of angiotensin II to aortic rings incubated in Krebs' Ringer bicarbonate medium produced tension generation (0.9 +/- 0.12 g = 100%). Treatment of aortic rings with simvastatin inhibited the angiotensin II-induced contraction 58 +/- 0.06%. To evaluate this effect further, dose-response curves with noradrenaline were measured in the presence and absence of 20 micromol/l simvastatin, lovastatin, mevastatin and pravastatin. The results indicate that simvastatin, lovastatin and mevastatin inhibited the contraction induced by noradrenaline (10 micromol/l) by about 50%. Pravastatin did not inhibit aortic ring contraction. Furthermore, the concentration required for 50% of the maximal contraction (EC50) by noradrenaline (6.2 +/- 0.1 nmol/l) was significantly increased by simvastatin, lovastatin, mevastatin and pravastatin. The inhibition of vascular contraction by vastatins appears to involve inhibition of 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase activity because the inhibitory effect of simvastatin was reduced 50% by 10 mmol/l mevalonic acid. To determine whether the depression of vascular contraction by these agents was correlated with cell calcium changes, the angiotensin II-induced calcium mobilization was determined in Fura-2 loaded cells, before and after treatment with these inhibitors. Simvastatin, lovastatin and mevastatin significantly reduced the angiotensin II-induced calcium mobilization. The concentration that induced 50% inhibition was 3.3 micromol/l for simvastatin, 17.4 micromol/l for mevastatin and 21.7 micromol/l for lovastatin. No effect of pravastatin on calcium mobilization was observed. CONCLUSIONS: These findings suggest that lactone vastatins depress vascular contraction by reducing cytosolic calcium release in vascular smooth muscle cells. These agents also appear to exert competitive and non-competitive type antagonisms on noradrenaline action.

Angiogenesis Inhibitors↗
PubMed1995

Readmission in unstable angina.

To determine the characteristics of patients re-admitted after unstable angina (UA) pectoris, 120 consecutive patients hospitalized due to primary UA pectoris were prospectively studied 22 +/- 3 months after discharge. The patients were grouped based on the readmission rate. Those in group A (50) had recurrent admissions (mean 2.6, range 2 to 5). Seventy patients (group B) did not have readmissions during the follow-up period. All patients underwent coronary angiogram and symptoms-limited exercise stress test before discharge. The univariate characteristics for readmission were: age over 70 years (p = 0.02), nondiagnostic exercise stress testing (p = 0.03), angiographically diffuse coronary artery disease (p = 0.004), and non-interventional management (P < 0.001). Patients readmitted had increased incidence of myocardial infarction (p = 0.004) but similar survival at 2 years. By regression analysis, important variables for readmission were non-interventional management (Chi-Square = 7.6, p = 0.01), non diagnostic treadmill test (Chi-Square = 6.9, p = 0.03) and diffuse coronary artery disease (Chi-Square = 6.2, p = 0.04). It is concluded that in the interventional era the most important factor for readmission after primary UA pectoris is non-interventional management. Coronary revascularization should not be denied solely on the basis of age.

Aged↗
PubMed1994

Opportunistic invasion of the heart in Hispanic patients with acquired immunodeficiency syndrome.

One hundred consecutive patients who died of the acquired immunodeficiency syndrome (AIDS) were studied with an emphasis on the heart. Thirty-two patients showed pathologic changes. The pathologic findings included infection by Histoplasma capsulatum, Toxoplasma gondii, Mycobacterium tuberculosis, cytomegalovirus. Cryptococcus neoformans, and atypical mycobacteria. Noninfectious pathologic findings included nonspecific myocarditis, focal necrosis, focal fibrosis, and acute subendocardial infarction.

AIDS-Related Opportunistic Infections↗
PubMed1994

[Enalapril reduces the degree of left ventricular remodeling after acute myocardial infarction and reduces the incidence of arrhythmia in ischemic disease].

The present study shows that enalapril prevents the excessive remodeling of the left ventricle after acute myocardial infarction. This randomized and double blind clinical study analysed 50 patients with an inferior myocardial infarction. The effect of enalapril was evaluated through cardiac volumes, ejection fraction, neurohormonal levels and incidence of the left ventricle disfunction after acute myocardial infarction. The patients treated with enalapril showed a significant reduction on the values of nor-epinefrine, angiotensine II, natriuretic hormone and vasopressine, four weeks after initiation of treatment. The ejection fraction and the level of the wall movement was more favourable, four weeks after infarction, in the group treated with enalapril. The incidence of congestive heart failure and arrhythmias was lower in the group treated with enalapril. So, we conclude that enalapril is a drug that prevents the excessive remodelling of the left ventricle after an acute myocardial infarction.

Aged↗
PubMed1994

Transient elevation of pulmonary arterial pressure induced by sublingual angiotensin converting enzyme inhibitors.

Twelve patients with ischemic heart disease had complete left and right catheterization before and after sublingual captopril. Hemodynamic measurements were ten (10) minutes apart and were monitored for thirty (30) minutes. The heart rate increased from 70 +/- 13 to 76 +/- 11 beats/minute (P = .04). There was no change in the arterial blood pressure, although the systemic vascular resistance decreased from 1500 +/- 400 to 1026 +/- 480 dynes-sec-cm-5 (P < .0001). The pulmonary artery pressure was increased 15 +/- 6 to 25 +/- 5mmHg (P = .005) and the pulmonary vascular resistance increased from 288 + 160 to 376 + 160 dynes-sec-cm-5 (P < .0001). The wedge pressure increased from 7 +/- 2 to 14 +/- 3 mmHg (P = .05). The cardiac output (CO) increased from 5.06 +/- 1.06 to 578 +/- 1.58 Lt/min. (P.05 =. The left ventricular end diastolic volume (LVEDV) increased from 128 +/- 40 to 145 +/- 37cc)P = .002), without change in the end systolic volume (ESV). The ejection fraction (EF) increased from 56 +/- 3 to 61 +/- 4% (P = .02). These pressure changes appeared at two (2) minutes and disappeared after thirty (30) minutes. The study shows that, sublingual captopril produces a transient elevation of the pulmonary artery pressure and resistance.

Administration, Sublingual↗
PubMed1994

Lack of interaction of angiotensin converting enzyme inhibitors with muscarinic and neuropeptide Y receptors.

In studies conducted in patients undergoing cardiac catheterizations, some hemodynamic changes were observed after the acute sublingual administration of the angiotensin converting enzyme inhibitors (ACEI) captopril, enalapril, and lisinopril. These changes consisted of an increase in pulmonary artery pressure, pulmonary vascular resistance (PVR) and induction of hypoxia. The pressure changes were transitory and disappeared after 25 min. The possible mechanisms involved in these changes may relate to interactions of the ACEI with peripheral receptor systems for hormones and neurotransmitters. We have thus undertaken the task of evaluating the potential effect of ACEI on biological receptor molecules. We have begun with studies on muscarinic receptors, and the recently characterized neuropeptide Y (NPY) receptors of endothelial cells. Equilibrium binding assays with 3H-QNB have been conducted for muscarinic receptors using rat brain synaptosomes, due to its expression of multiple muscarinic receptors subtypes. In addition 125BH-NPY binding assays were conducted on intact adrenal medullary endothelial cells. Enalapril and captopril, 10(-7) to 10(-3) M, were not able to produce significant inhibition of either muscarinic or NPY receptor probes. The paradoxical changes elicited by sublingual ACEI seems not to involve interaction with muscarinic or NPY receptors.

Adrenal Medulla↗
PubMed1993

Effects of enalaprilat on hemodynamics and ventricular activation duration in hypertensive patients with left ventricular hypertrophy: clinical evidence of improved excitation-contraction coupling with angiotensin converting enzyme inhibition in human hypertension.

Hypertension is a major risk factor for the development of heart failure. Despite significant progress in our knowledge of the physiopathology of heart failure, the cause for decompensation in patients with left ventricular hypertrophy (LVH) is still obscure. The angiotensin converting enzyme inhibitor enalaprilat has been found to improve electromechanical coupling of heart cells in animal models. To assess the effects of enalaprilat on ventricular electromechanical coupling in humans, we studied the His bundle electrograms and hemodynamics in 22 hypertensive patients with LVH. Patients received either 2.5 mg enalaprilat or saline placebo intravenously in a double-blind protocol. There were no significant changes in heart rate, and atrioventricular and His-Purkinje conduction times. Ventricular activity duration was reduced from 110 +/- 11 msec to 88 +/- 13 msec after enalaprilat administration (P < .01). Enalaprilat decreased peak-systolic and end-diastolic left ventricular pressures, and arterial and pulmonary pressures, as well as pulmonary and systemic vascular resistances. End-systolic wall stress decreased 18% (P < .01), ejection fraction increased 11% (P < .01), and end-diastolic pressure-volume ratio decreased 50% (P < .001) after enalaprilat administration. There were no significant changes in these parameters after saline infusion. It is concluded that enalaprilat reduces ventricular activation duration and improves ventricular performance in hypertensive patients with LVH. Data suggest that enalaprilat significantly improves excitation-contraction coupling in these patients.

Action Potentials↗
PubMed1993

Effects of enalapril on ventricular volumes and neurohumoral status after inferior wall myocardial infarction.

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system and its beneficial modification with the use of angiotensin-converting enzyme inhibin after inferior wall myocardial infarction (MI) was evaluated. Fifty patients with acute inferior MI were randomly assigned to receive 5 mg per day of either enalapril or placebo after admission. Blood tests for neurohormone levels and echocardiograms were performed at initial examination and 4 weeks later. Baseline characteristics were similar in the two groups. Four weeks after randomization, patients treated with enalapril had lower end-diastolic volume (146 +/- 29 vs 167 +/- 15 ml; p = 0.04), end-systolic volume (56 +/- 18 vs 107 +/- 17 ml; p = 0.03), serum norepinephrine levels (320 +/- 93 vs 465 +/- 77 pg/ml; p < 0.01), angiotensin II levels (18 +/- 6 vs 54 +/- 11 pg/ml; p < 0.01), and atrial natriuretic polypeptide levels (106 +/- 9 vs 122 +/- 17 pg/ml; p = 0.05) than patients given placebo. The incidence of heart failure after MI was also lower in this group (4% vs 16%; p = 0.009). Results show that there is early neurohumoral activation in the course of acute inferior wall MI. Enalapril reduces neurohumoral levels and preserves ventricular volumes. These effects were associated with a reduction in the incidence of heart failure 4 weeks after MI in these patients.

Aged↗
PubMed1993

Cocaine induced myocardial ischemia.

We report a case of myocardial ischemia induced by cocaine. The ischemia probably induced by coronary artery spasm was reversed by nitroglycerin and calcium blocking agents.

Adult↗
PubMed1992

Reduction in cardiac conduction velocity delay by angiotensin converting enzyme inhibition in hypertensive patients with left ventricular hypertrophy. Detection by signal averaged electrocardiography.

Hypertensive patients with left ventricular hypertrophy (LVH) have increased prevalence of ventricular arrhythmias. Slow conduction velocity at the level of hypertrophic myocardial cells has been one of the postulated mechanisms for these arrhythmias. To assess the effects of angiotensin converting enzyme inhibition on modification in ventricular conduction velocities, we studied 25 hypertensive patients with LVH using signal averaged electrocardiography (SAECG) in a randomized double-blind placebo controlled and cross-over trial. Data were acquired at baseline and 10 min after a double-blind intravenous infusion of saline placebo or 2.5 mg enalaprilat. Sequential cross-over was done the next day. Root mean square vector was 55 +/- 5 microV at baseline, 55 +/- 5 microV after placebo and 54 +/- 4 microV after enalaprilat (P = NS). Low amplitude signal < 40 msec was 45 +/- 4 msec at baseline, 45 +/- 4 msec after placebo, and 43 +/- 4 msec after enalaprilat (P = NS). There was no change in filtered QRS (fQRS) duration between baseline (113 +/- 10 msec) and placebo (113 +/- 11 msec) measurements. However, after enalaprilat infusion, there was a significant reduction in fQRS to 106 +/- 7 msec (P = .04), and five patients (20%) with late potentials had normalization of this feature (P = .001). The data suggest that angiotensin converting enzyme inhibition with enalaprilat reduces conduction velocity delay in hypertensive patients with LVH.

Adult↗
PubMed1992

Effects of enalapril on heart failure in hypertensive patients with diastolic dysfunction.

Ten hypertensive patients with symptoms of heart failure and normal systolic function but with diastolic dysfunction were treated with 10 mg enalapril twice a day for 9 +/- 3 months to evaluate the effects of this agent alone on heart failure induced by diastolic dysfunction. After therapy, all patients improved and echocardiographic parameters of diastolic dysfunction became normalized. It is concluded that enalapril appears to be useful in the treatment of heart failure in hypertensive patients with normal systolic function and diastolic dysfunction.

Adult↗
PubMed1992

Enalapril increases cardiac refractoriness.

The influence of enalapril--an angiotensin converting enzyme inhibitor--on cardiac refractoriness was investigated. Strength-interval curves were initially obtained under control conditions and after exposing the muscles to Tyrode solution containing 50 micrograms/ml of enalapril. The results indicate that enalapril displaced the strength-curves to the right. The minimal current intensity required to elicit a propagated response was clearly increased by enalapril at all the intervals used. No change in action potential duration was found with enalapril but the action potential amplitude and the resting potential were both increased. The rise in cardiac refractoriness caused by enalapril might indicate that the drug has anti-arrhythmic properties.

Action Potentials↗