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Biomedical subjects

F Navarro-Lopez

Publications and source records attributed to F Navarro-Lopez.

17 recordsLinked to original sources
PubMed1993

Class III actions in an experimental model of ventricular tachycardia.

Simplified models of re-entry may help in our understanding of the electrophysiologic effects of class III drugs. In a model of re-entrant ventricular tachycardia around a ring of epicardium in Langendorff-perfused rabbit hearts, the electrophysiologic effects of class III antiarrhythmic drugs were studied and compared to those of class I drugs. Class III drugs were effective in terminating fast re-entrant ventricular tachycardias. Prolongation of the refractory period without affecting conduction velocity resulted in a closure of the excitable gap and collision of the head of the propagating impulse against its own tail of refractoriness. In slow ventricular tachycardias, despite a similar increase in refractory period, the excitable gap remained large enough to allow perpetuation of the tachycardia.

Animals↗
PubMed1993

The complexity of mechanisms in ventricular tachycardia.

Several pathophysiological substrates may be responsible for ventricular tachycardia (VT) occurring in the chronic phase of a myocardial infarction. Reentrant circuits can have anatomical or functional characteristics. Macroreentrant or microreentrant circuits have been described. Activation maps have shown that the circuit can be represented as a single loop or as a figure-of-eight reentrant pattern. All these different substrates have in common that they result in sustained monomorphic VT. The adequate treatment will probably be different for each one of them. In this article, some possible pathophysiological substrates of VT occurring in the chronic phase of a myocardial infarction are reviewed. Finally, we speculate on how catheter ablation may modify each one of the substrates.

Catheter Ablation↗
PubMed1993

Left ventricular hypertrophy in asymptomatic essential hypertension: its relationship with aldosterone and the increase in sodium-proton exchanger activity.

In order to analyse the hormonal and erythrocyte ion transport systems in relation to left ventricular hypertrophy (LV) in essential hypertension, a prospective study of 50 consecutive hypertensive patients under 55 years of age and without prior antihypertensive therapy was performed. Twenty-seven normal subjects with no family history of hypertension served as controls. LV hypertrophy, as assessed by echocardiography, was present in 64% of the hypertensive patients. This showed an increase (P < 0.001) in intra-erythrocyte Na+ concentration (8.1 +/- 1.2 vs 6.9 +/- 1 mmol.l-1.cells-1) and Na+:H+ exchange activity (8.8 +/- 4 vs 5.5 +/- 1.3 mmol.[l.cells.h-1]). There was a significant association between plasma aldosterone levels (19.1 +/- 12 ng.dl-1) with intra-erythrocyte Na+ content (r = 0.370, P < 0.05) and Na+:H+ exchange activity (r = 0.385, P < 0.01) as well as with echocardiographic LV mass index (138 +/- 40 g.m-2, r = 0.393, P < 0.01). The results are consistent with the concept that increased entry of Na+ into cells via Na+:H+ exchange could be a determining factor in left ventricular hypertrophy, which might be influenced by aldosterone.

Adult↗
PubMed1989

The effects of alcoholism on skeletal and cardiac muscle.

To determine the prevalence of alcoholic myopathy and cardiomyopathy, we studied a group of 50 asymptomatic alcoholic men (mean age, 38.5 years) entering an outpatient treatment program. Studies performed included an assessment of muscle strength by electronic myometer, muscle biopsy, echocardiography, and radionuclide cardiac scanning, with comparison to healthy control subjects of similar age. The patients' mean (+/- SEM) daily alcohol consumption was 243 +/- 13 g over an average of 16 years. These patients had no clinical or laboratory signs of malnutrition or electrolyte imbalance. Forty-two percent of the patients, as compared with none of the controls, had strength of less than 20 kg as measured in the deltoid muscle. Muscle-biopsy specimens from 23 patients (46 percent) had histologic evidence of myopathy. In the cardiac studies, when the alcoholic patients were compared with 20 healthy controls, the patients had a significantly lower mean ejection fraction (59 vs. 67 percent), a lower mean shortening fraction (33 vs. 38 percent), a greater mean end-diastolic diameter (51 vs. 49 mm), and a greater mean left ventricular mass (123 vs. 106 g per square meter of body-surface area). One third of the alcoholics had an ejection fraction of 55 percent or less, as compared with none of the controls. Endomyocardial biopsy specimens from six patients with ejection fractions below 50 percent showed histologic changes of cardiomyopathy. The estimated total lifetime dose of ethanol correlated inversely with muscular strength (r = -0.65; P less than 0.001). In an analysis that also included six patients with symptomatic alcoholic cardiomyopathy, the estimated total lifetime dose of ethanol correlated inversely with the ejection fraction (r = -0.58; P less than 0.001) and directly with the left ventricular mass (r = 0.59; P less than 0.001). We conclude that myopathy of skeletal muscle and cardiomyopathy are common among persons with chronic alcoholism and that alcohol is toxic to striated muscle in a dose-dependent manner.

Adult↗
PubMed1986

Systolic compression of coronary artery in hypertrophic cardiomyopathy.

To determine the prevalence and significance of the systolic compression of the anterior descending coronary artery in hypertrophic cardiomyopathy, we studied 54 consecutive patients out of a catheterization laboratory population of 1619. This angiographic finding was found to be more prevalent (P less than 0.001) and severe in myopathic than in secondary hypertrophy. Complete systolic occlusion occurred in 5 of the 6 patients with nonobstructive cardiomyopathy showing the systolic narrowing. Severe septal squeezing was also present in these cases and the diastolic time lag to refill the distal branches reached 20-33% of the diastolic period. This subset of patients showed the least dynamic anterior wall contraction (P less than 0.001) and the highest incidence of thallium-201 perfusion defects (P less than 0.05) and of recurrent cardiac arrest (P less than 0.05). We conclude that severe systolic compression of the descending coronary artery in hypertrophic cardiomyopathy may be an angiographic marker of the myopathic hypertrophy extending to the anterior wall and might contribute to ischemia when the time to restore the distal perfusion is greatly delayed.

Adolescent↗
PubMed1983

Prevalence and prognosis after a first nontransmural myocardial infarction.

Prevalence, prognosis, and coronary anatomy associated with nontransmural myocardial infarction (MI) were prospectively assessed in 458 consecutive men admitted to our coronary care unit with a first MI. Cardiac catheterization was performed in 402 of the 436 survivors within 1 month of the acute event. Mean follow-up was 33 months (range 5 to 72). Nontransmural MI was diagnosed in 28 patients (6%). These patients were younger (46 +/- 10 versus 51 +/- 7 years, p less than 0.001) and had lower peak creatine kinase values (601 +/- 319 versus 1,141 +/- 923 U, p less than 0.01) and better ejection fraction (63 +/- 8 versus 46 +/- 14, p less than 0.001) than did their counterparts. Survivors of nontransmural MI also had fewer affected arteries (p less than 0.001) and a lower prevalence of total or subtotal occlusion (greater than 90%) in the involved artery (p less than 0.01). Mortality in the acute phase and long-term survival at 4 years (Kaplan-Meier) in patients with nontransmural MI (94%) were similar to those in patients with transmural MI (90%). The occurrence of new nonfatal coronary events was also similar in both groups of MI survivors. Thus, in the absence of symptoms, more aggressive management to improve survival does not seem warranted after nontransmural MI.

Adult↗
PubMed1982

Angiographic findings 1 month after myocardial infarction: a prospective study of 259 survivors.

Coronary anatomy as it relates to left ventricular function was assessed prospectively in patients who survived acute myocardial infarction. The study population included 259 consecutive male patients age 60 years or younger who underwent catheterization 30 days after the acute event. Coronary artery obstructive lesions (greater than 50% reduction in luminal diameter) were found in 241 patients (93%), 118 (45%) of whom had total and 76 (29%) subtotal (greater than 90%) stenosis) occlusion of at least one coronary artery. Normal coronary vessels were seen in eight patients (3%) and nonobstructive lesions in 10 (4%). One-, two- and three-vessel disease were present in 89, 86 and 66 patients, respectively. Patients with normal coronary arteries or nonobstructive lesions had higher ejection fractions than those with obstructive lesions in one, two or three vessels (p less than 0.05). Ejection fraction was lower (p less than .001) and the percentage of akinetic segments higher (p less than 0.001) in patients with total or subtotal lesions and no collaterals. Adequate collaterals, seen in 29 patients (11%), significantly improved regional wall motion (p less than 0.05) and decreased the percentage of akinetic segments (p less than 0.001). Thus, in a substantial number of patients (32% in our series), the infarcted area is spontaneously reperfused by collaterals or through the involved artery. Both mechanisms ameliorate wall motion in corresponding areas.

Collateral Circulation↗
PubMed1981

Myocardial infarction with normal coronary arteries: a prospective clinical-angiographic study.

The association of myocardial infarction with normal coronary arteries was analyzed prospectively. A series of 259 consecutive men aged 60 years or less underwent selective coronary angiography 30 days after a definite infarct. Coronary arterial lesions were documented in 251 patients, normal coronary arteries in the remaining 8. The latter patients had a significantly lower (p less than 0.001) mean age than the former; no patient older than 50 years had patent coronary arteries, whereas 5 of the 11 patients under age 35 had normal arteries. The prevalence of risk factors was similar in both groups of patients. Although there were no group differences in infarct size or location, patients with normal coronary arteries had a higher ejection fraction (p less than 0.01) and a lower left ventricular end-diastolic pressure (p less than 0.05). A previous history of angina or infarction and the occurrence of new coronary events were confined to patients with coronary arterial lesions. The clinical course of patients presenting with normal angiograms was uneventful. Transient coronary occlusion, the most likely mechanism of infarction in this group of patients, could not be ascribed to either spasm or platelet hyperactivity.

Blood Platelets↗
PubMed1981

Disabling angina pectoris with normal coronary arteries in patients undergoing long-term hemodialysis.

Reports of patients undergoing long-term hemodialysis presenting with angina pectoris have usually shown severe coronary atherosclerosis. We studied a series of nine patients undergoing regular maintenance dialysis referred for incapacitating angina. Of them, four had strictly normal coronary angiograms. The patients with normal angiograms were all females who were significantly younger (p less than 0.05) and had more severe hypertension and higher left ventricular wall stress than patients showing coronary artery lesions. Anemia and increased myocardial oxygen consumption due to high blood pressure may explain the syndrome of angina pectoris in the presence of long-term dialysis in patients with normal coronary arteries. The prevalence of this association cannot be ascertained unless prospective studies are conducted. However, our data suggest that it might not be an uncommon finding.

Adult↗
PubMed1980

Relief of angina by periarterial muscle resection of myocardial bridges.

A 47-year-old man presented with exertional angina. Selective coronary arteriography showed complete systolic segmental occlusion of the left anterior descending coronary artery producing milking effect. Permanent relief of symptoms was achieved by surgical excision of myocardial bridges. Postoperative angiography performed 11 months later was normal. Periarterial muscle resection should be considered in symptomatic patients with this rare anomaly.

Angina Pectoris↗
PubMed1980

Restrictive cardiomyopathy in pseudoxanthoma elasticum.

A unique case of severe and diffuse endocardial fibroelastosis covering the entire left ventricle and associated with pseudoxanthoma elasticum is presented. The clinical picture was that of an apparently primary restrictive cardiomyopathy. Specific histologic lesions could be recognized in the endocardium.

Adult↗
PubMed1978

Isolated T wave alternans.

Two patients with isolated T wave alternans are reported, with their vectocardiograms, their response to carotid sinus stimulation, and the response to calcium infusion in one of them with documented severe hypocalcemia. Eleven cases of the literature are briefly reviewed. The alternans of the T wave appears with severe QT prolongation, QT alternans, and an increased tendency to ventricular fibrillation. The findings are consistent with the hypothesis that T wave alternans may be the electrocardiographic manifestation of the transmembrane action potential alternans and could be related in some cases to hypocalcemia.

Adolescent↗
PubMed1978

Isolated T wave alternans elicited by hypocalcemia in dogs.

Isolated T wave alternans (TWA) could be consistently induced in 13 dogs by infusion of an acid dextrose solution (ACD) and in nine with a 2% EDTA disodium solution. To study the factors concerned in evoking TWA, serial determinations of total and ionized serum calcium (ICa), Mg, K, pH, pCO2 and pO2 were performed. Arterial or LV pressures and LV dp/dt as well as a standard electrocardiographic lead were monitored. TWA appeared after the QT interval was significantly prolonged and was associated with a fall in LV pressure and with mechanical alternans. QT alternans could also be detected in 50% of the cases. ICa levels were significantly reduced at the moment of appearance of the TWA. Data obtained support the conclusion that TWA was the result of a reduction in the level of the ICa, probably interfering with the calcium transport mechanisms of the myocardial cell, although the possibility that the alternans may be due to other effects of the two agents employed unrelated to calcium lowering cannot be excluded.

Animals↗