ST segment alternans in vasospastic angina.
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Biomedical subjects
Publications and source records attributed to M Condorelli.
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Baroreceptor function was assessed by (1) the reflex response during Valsalva maneuver, (2) phenylephrine injection, and (3) increase in neck tissue pressure by a neck-chamber in 15 borderline hypertensives (B) and in 15 age-matched normotensives (N). B responded to the fall in blood pressure, occurring in phase II of Valsalva maneuver, with an increase in blood pressure and a decrease in the R-R interval of comparable extent to those observed in normals. On the contrary, in phase IV B showed a depressed heart rate reflex response whether evaluated by the slope of the regression line obtained by plotting the R-R interval versus the systolic blood pressure (slope: B = 6.1 +/- 3.3; N = 35.6 +/- 7, p less than 0.005) or by the change in R-R interval (delta R-R interval: B = 67.5 +/- 37 ms; N = 319 +/- 55 ms, p less than 0.005). On the other hand, both phenylephrine injection and neck-chamber procedure showed an impaired baroreflex responsiveness in B. A linear positive correlation was found between the individual values of the slopes obtained during phase IV of Valsalva maneuver and after phenylephrine injection both in N (r = 0.944, p less than 0.001) and in B (r = 0.84, p less than 0.001). Finally, a linear positive correlation was found between the individual values of the slopes obtained by the phenylephrine technique and the corresponding maximum percent change in R-R interval during phase IV of the Valsalva maneuver both in normals and in hypertensives. In conclusion, overshoot bradycardia during Valsalva maneuver seems to show enough specificity in the evaluation of baroreflex responsiveness to be employed in epidemiological studies in this area.
Development of bilateral ventricular hypertrophy in animals exposed to sustained hypoxia is demonstrated. Female Sprague-Dawley rats (180-200 g) were subjected to acute (0.40 atm/24 h) or chronic intermittent (0.40 atm/18 h/day/7days) hypobaric hypoxia. Control animals were maintained at room pressure. The changes in ventricular mass (right ventricle and left ventricle including the septum) were evaluated on the basis of the dry weight values immediately at the end of hypoxic stimulus. Data show that both acute and chronic hypobaric hypoxia allow rate to develop a significantly degree of hypertrophy in the left as well as in the right ventricle. The factors involved in the genesis of the left ventricular hypertrophy in hypoxic conditions are presented.
It has been demonstrated that, in most arteriopathic patients, vasodilators induce the vascular steal phenomenon, i.e. the shunting of blood from the ischemic to the normally perfused areas. It is conceivable, therefore, that vasoconstrictors may improve in the opposite way, reducing the blood flow to the normal zones and increasing it to the ischemic. A "reverse vascular steal" caused by the simultaneous IV injection of a vasodilator and a beta-blocker has been previously shown; however, the chronic treatment of arteriopathic patients with beta-adrenoceptor blocking drugs often results in increased evidence of peripheral arterial insufficiency; therefore, the combination of a vasodilating drug with a beta-blocker is limited in the clinical practice. The aim of this study was to investigate the efficacy of the combination of the vasodilator papaverine hydrochloride with a drug having vasoconstrictive action without the undesirable side effects of beta-blockers. Accordingly, raubasine (40 mg) was given p.o. associated with papaverine (300 mg) in 10 arteriopathic patients, who presented a significant reduction of blood flow in the affected limb after the administration of 300 mg p.o. of papaverine alone. The measurements of blood flow were performed by impedance plethysmographic recordings to evaluate papaverine plasma concentrations. Data obtained by this study indicate that papaverine alone induces a significant reduction of blood flow starting from the time of its maximal plasma concentration. Raubasine alone does not induce any change in blood flow, while the combination of the 2 drugs significantly increases the blood supply to the affected limb. These favorable results, probably related to the ability of raubasine to induce a reverse vascular steal, suggest that the combination of this drug with a vasodilator such as papaverine may represent a new approach in the treatment of peripheral arterial insufficiency.
The effects of intravenous administration of several quinidine-like antiarrhythmic drugs (bunaftine, monochloroacetyl ajmaline, lidocaine, mexiletine, disopyramide, aprindine, diphenylhydantoin, procainamide) on left ventricular performance, evaluated by systolic time intervals (STI), were studied in 100 patients with atherosclerotic heart disease. The STI were measured: the pre-ejection period (PEP), the isometric contraction time (ICT), the left ventricular ejection time (LVET), corrected LVET (LVETc), and the PEP/LVET ratio. The degree of impairment of left ventricular performance was maximal after aprindine and disopyramide administration. This was demonstrated by significant increases in the PEP, ICT, and PEP/LVET and by significant decreases in LVET and LVETc, in patients in both III-IV and I-II NYHA classes. Bunaftine, monochloroacetyl ajmaline, and lidocaine induced a less marked impairment of myocardial performance, since the PEP, ICT, and PEP/LVET increases were not significant compared to controls in patients in NYHA class I-II, and since no variation of LVET and LVETc were observed. Mexiletine effects on myocardial performance appear to be intermediate between these groups of drugs. Diphenylhydantoin and procainamide, considered separately because of their effects on heart rate and blood pressure which are not possessed by the other drugs, induced significant increases of PEP in NYHA class III-IV patients. However, the effects of these 2 drugs on myocardial performance may have been underestimated, due to the concomitant hemodynamic effect of these drugs.
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The authors investigated the changes in cardiovascular and splanchnic hemodynamic, diuresis and urinary and hepatic veins osmolarity induced by hypotonic water load in five normal subjects and in five patients with congestive heart failure (CHF). Pulmonary wedge pressure increased significantly only in CHF patients while cardiac index, total pulmonary resistances and peripheral vascular resistances remained unchanged in both groups. Hepatic blood flow increased significantly in control group while in CHF showed a significant reduction 15 and 30 minutes after water load. Hepatic veins osmolarity decreased significantly in control group only at the 45th minute. Diuresis was significantly higher in normals which eliminated water load with a lower urinary osmolarity. The authors conclude that: water loading is particularly interesting in so much it resembles the physiological conditions of the absorption of the alimentary hypotonic bolus; the failing heart responds to the water load on a depressed function curve; the hepatic blood flow is reduced in CHF patients and is probably responsible for some humoral abnormalities found in these subjects; CHF patients eliminate a water load slower than a normal subject and with a higher osmolarity.
This study was undertaken to evaluate the efficacy of coronary artery by-pass grafting (CABG) in elderly patients with coronary artery disease. A consecutive series of 79 patients, 65 years of age and older, who underwent CABG from 1975 to 1981 was analysed and their follow up status ascertained. This group was compared with a consecutive series of 397 patients under the age of 65 who underwent CABG during the same period. The patients aged 65 years or greater had a higher incidence of unstable angina pectoris (p less than 0.05). Coronary angiographic and left ventriculographic features were comparable in both age groups; also comparable were the number of saphenous veins graft utilized and the number of left ventricular aneurysmectomies and mitral valve replacements performed. The hospital mortality rate for patients aged 65 years and older was 12.6%, for those aged less than 65, it was 8.3%; if the other cardiac procedures are excluded mortality rates become 12.5% and 6.0% respectively (n.s.). Survival at 6 years was 92% for patients in both age groups. However, the symptomatic status was less favourable in older patients, compared with that obtained in younger patients (p less than 0.05).
We have studied the role of arachidonic acid (AA) metabolism in the release of lysosomal enzymes (beta-glucuronidase and lysozyme) from human polymorphonuclear leukocytes (PMNs). 5,8,11,14-Eicosatetraenoic acid (ETYA), which inhibits both the cyclo-oxygenase and the lipoxygenase pathways of AA metabolism, was found to cause a dose-dependent inhibition of lysosomal enzyme release from human PMNs induced by immunological (i.e., serum-treated zymosan: Zx) and nonimmunological stimuli (i.e., formyl methionine-containing peptide and the Ca2+ ionophore A23187). In contrast, the non-steroidal anti-inflammatory drugs (indomethacin, meclofenamic acid and aspirin), which only block the cyclo-oxygenase pathway of AA metabolism, had little effect on enzyme release from PMNs induced by the same stimuli. 5,8,11-Eicosatriynoic acid (ETI), a selective inhibitor of the lipoxygenase pathway of AA metabolism, caused a dose-dependent inhibition of lysosomal enzyme release elicited by Zx, f-met peptide, and A23187. p-Bromophenacyl bromide (BPB), which inhibits the phospholipase A2 (PLA2) activity in several tissues, was found to cause a dose-dependent inhibition of lysosomal enzyme release induced by the same immunological and non-immunological stimuli. The inhibitory effect of BPB on enzyme release was irreversible and extremely rapid. It appears that activation of PLA2 and the products of the AA metabolism, generated via a lipoxygenase pathway, play an essential role in the biochemical control of human PMNs activation and secretion.
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1. The effects of intravenous administration of neostigmine and propranolol, individually or in combination, on baroreflex responsiveness have been evaluated in 18 borderline hypertensive subjects and in 14 age-matched control subjects. 2. Baroreceptor sensitivity was tested by evaluating both heart rate response to phenylephrine-induced increase in arterial pressure, and heart rate and blood pressure changes induced by increasing neck-tissue pressure by means of a neck-chamber. 3. In borderline hypertensive subjects a reduced baroreflex responsiveness was demonstrated with both stimuli as compared with normal subjects. Neostigmine administration improved consistently both reflex responses. Similarly, after propranolol treatment, borderline hypertensive subjects showed a significant enhancement of the baroreflex sensitivity. Finally, the combined administration of neostigmine and propranolol restored the baroreflex responses. In fact, both the mean slopes of the regression lines between blood pressure and R-R interval after phenylephrine and the increase in mean arterial pressure and heart rate induced by the reduction in carotid transmural pressure in borderline hypertensive subjects were similar to those observed in normals. 4. These findings indicate that in borderline hypertensive subjects the impairment of baroreflex responsiveness is mainly due to abnormalities of autonomic regulation.
The effect of oral salt loading (400 mmol per day of NaCl for 7 days) on cardiac and pancreatic beta-receptor responsiveness has been evaluated in 12 patients with established essential hypertension and in seven age-matched control subjects. Cardiac beta-receptor responsiveness was evaluated by assessing the dose of isoprenaline which increased a stable heart rate by 25% (chronotropic dose 25%, CD 25%). Pancreatic beta-receptor responsiveness was measured by the incremental areas of insulin secretion induced by iv infusion of increasing amounts of isoprenaline. Before salt load, CD 25% was significantly higher in hypertensives compared with controls (7.84 +/- 1.34 micrograms vs 3.9 +/- 0.48 micrograms, P less than 0.05) while there was no difference in the isoprenaline-induced insulin secretion between the two groups of subjects. After salt loading, CD 25% was significantly reduced in hypertensive patients but was not modified in normal subjects. Therefore, the difference in CD 25% was no longer detectable between the two groups (5.5 +/- 1.42 micrograms vs 3.2 +/- 0.48 micrograms in normal subjects and in hypertensives, respectively, NS). Furthermore, salt loading failed to induce any change in isoprenaline-induced insulin secretion in either groups. These results support the existence of a relationship between sodium intake and adrenergic beta-receptor responsiveness in human hypertension.
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