PubMed Health⌕ Search

Biomedical subjects

M Metra

Publications and source records attributed to M Metra.

At least 37 records · Page 2Linked to original sources

Electrolyte disturbances in chronic heart failure: metabolic and clinical aspects.

The pathophysiology of congestive heart failure (CHF) includes conditions (e.g., activation of the renin-angiotensin-aldosterone system) which, when combined with CHF therapies, make patients afflicted with this syndrome quite susceptible to electrolyte disturbances. The most commonly encountered are hyponatremia, hypokalemia, and hypomagnesemia. These derangements are of vast clinical importance; their development not only represents an immediate threat to the CHF patient (e.g., dysrhythmias secondary to hypokalemia), but are also indicative of underlying pathophysiologic events, an unfavorable clinical course, and occasionally an adverse therapeutic response. The optimal care of CHF patient includes the recognition and management of these electrolyte disturbances.

Chronic Disease↗

Clinical efficacy of ibopamine in patients with chronic heart failure.

Ibopamine, the most widely studied dopaminergic drug for the treatment of chronic heart failure, appears to have beneficial hemodynamic, renal, and neurohormonal effects in this setting. Angiotension-converting enzyme (ACE) inhibitors have become the recommended standard treatment for chronic heart failure; however, some patients may benefit from additional drugs to improve their symptoms and functional capacity. Ibopamine may be effective as an additive drug for patients with chronic heart failure. It is also possible that ibopamine will improve survival in these patients. Large-scale trials are needed to assess the effects on morbidity and mortality when ibopamine is added to ACE inhibitors, diuretics, and possibly digitalis.

Clinical Trials as Topic↗

Dopaminergic drugs in congestive heart failure: hemodynamic and neuroendocrine responses to ibopamine, dopamine, and dihydroergotoxine.

Ibopamine has hemodynamic and neurohumoral effects potentially useful for the treatment of congestive heart failure (CHF), but its mechanism of action is not completely clear. To evaluate the role of dopaminergic receptor stimulation in the hemodynamic and neurohumoral activity of ibopamine, we compared the effects of ibopamine, 100 mg orally (p.o.) with those of the dopamine 2, 4, and 6 micrograms/kg/min intravenously (i.v.) and of the DA2 agonist dihydroergotoxine 6 micrograms/kg i.v. in 13 patients with chronic CHF [left ventricular ejection fraction (LVEF) < or = 35%]. All patients underwent right heart Swan-Ganz catheterization with determination of hemodynamic parameters at baseline, after 30 min of infusion of each dose of dopamine (DA) and < or = 6 h after ibopamine and dihydroergotoxine administration. Blood samples for the assessment of plasma renin activity (PRA), aldosterone, norepinephrine (NE), and epinephrine (Epi) were also obtained. Ibopamine induced a peak 21% increase of cardiac index (CI) with a 23 and 25% increase in stroke volume (SV) and stroke work indexes (SWI), respectively, and an 18% reduction in systemic vascular resistance (SVR). Similar changes were observed after DA infused at the doses of 2 and 4 micrograms/kg/min, whereas with the dose of 6 micrograms/kg/min heart rate (HR) increased by 23% and SV index (SVI) did not change further. Dihydroergotoxine administration induced only a significant 9% decrease in mean arterial pressure (MAP), with a 13% reduction in SVR.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

[Coronary angioplasty in chronic total occlusion: angiography results, complications, and predictive factors].

The results of coronary angioplasty of chronic total occlusions are still controversial. We examined baseline clinical and angiographic parameters and the success and complication rates of 142 consecutive procedures of coronary angioplasty of chronic occlusions selected among 1084 total procedures performed between January 1989 and May 1993. Procedural success was obtained in 109 procedures (77%) with 4 major cardiac complications (2.8%) consisting in one cardiac death caused by left main artery occlusion following an attempt of dilatation of an occluded left anterior descending artery, two non Q wave myocardial infarctions caused by distal embolization and one cardiac tamponade following artery perforation, successfully treated by pericardiocentesis. Extensive coronary dissection occurred in 24 procedures (17%): 5 caused vessel reocclusion and 19 were successfully treated by prolonged balloon inflation and/or use of long balloons or stent implantation. Among 15 baseline clinical and angiographic variables, none was predictive of cardiac complications or coronary artery dissection. In contrast, procedural success was significantly related with absence of bridging collaterals, duration of occlusion < 3 months and a tapered or thrombotic morphology of occlusion. Presence or absence of collaterals was the most significant variable selected by multivariate discriminant analysis. When patients with bridging collaterals were excluded from the analysis, occlusion morphology was the most important determinant. Success rates were 95% and 82% in patients with a tapered morphology lesion with < 3 months and > 3 months duration, respectively (ns); in contrast, success rates were 79% and 36% in patients with abrupt occlusion morphology of < and > 3 months duration (p = 0.001).

Adult↗

Clinical relevance and management of the major electrolyte abnormalities in congestive heart failure: hyponatremia, hypokalemia, and hypomagnesemia.

Electrolyte disturbances are a common complication of CHF. CHF provides a perfect milieu for the development of these disturbances; renal dysfunction, elevation of neurohormonal substances, activation of the renin-angiotensin-aldosterone axis, and diuretic therapy represent the major contributory factors. Hyponatremia is closely aligned with an unfavorable clinical course. Hypokalemia is associated with increased ventricular dysrhythmias. Hypomagnesemia noted in advanced CHF can be accompanied by arrhythmias and refractory hypokalemia. CHF also offers the ideal milieu (diseased, ischemic, and arrhythmogenic myocardium; elevated catecholamines; and arrhythmogenic drugs) for the threatening clinical consequences (clinical deterioration, dysrhythmias, or death) of these disturbances. These consequences underscore the importance of the recognition, appreciation, and management of these electrolyte abnormalities.

Heart Failure↗

Effects of short- and long-term carvedilol administration on rest and exercise hemodynamic variables, exercise capacity and clinical conditions in patients with idiopathic dilated cardiomyopathy.

OBJECTIVES: The study evaluated the effects of short- and long-term administration of carvedilol in patients with idiopathic dilated cardiomyopathy. BACKGROUND: Carvedilol is a beta-adrenergic blocking agent with vasodilator activity that might be well tolerated in patients with heart failure. METHODS: Forty patients with idiopathic dilated cardiomyopathy treated with digoxin, furosemide and angiotensin-converting enzyme inhibitors were randomized in a double-blind manner to receive either placebo or carvedilol. Right heart hemodynamic variables were evaluated up to 8 h after short-term drug administration and, on the next day, during cardiopulmonary exercise testing before and 3 h after drug ingestion. Placebo or carvedilol was added to standard therapy, starting with a dose of 6.25 mg twice a day with weekly increments up to the maximum of 25 mg twice a day. Patients were reevaluated after 4 months by cardiopulmonary exercise testing and measurement of right heart hemodynamic variables 12 h after last drug ingestion and 3 h after drug readministration. Left ventricular ejection fraction and volume, measured by equilibrium radionuclide ventriculography, quality of life and submaximal exercise duration were assessed before and after long-term therapy. RESULTS: Compared with placebo, carvedilol produced a short-term reduction in heart rate and pulmonary artery and pulmonary wedge pressures and, after long-term administration, increased both rest and peak exercise cardiac, stroke volume and stroke work indexes, with a further reduction in right atrial, pulmonary artery and pulmonary wedge pressures. Long-term carvedilol administration also improved rest left ventricular ejection fraction (from 20 +/- 7% to 30 +/- 12%, p < 0.001), submaximal exercise capacity, quality of life and New York Heart Association functional class. No baseline variable was predictive of the response to therapy. CONCLUSIONS: Short-term carvedilol administration reduces heart rate and mean pulmonary artery and pulmonary wedge pressures, whereas it improves both long-term rest and exercise left ventricular systolic function, reduces heart failure symptoms and improves submaximal exercise tolerance in patients with idiopathic cardiomyopathy.

Adrenergic beta-Antagonists↗

Pulmonary hypertension and systemic hypotension as limitations to exercise in chronic heart failure.

The authors have previously shown that the resistance ratio (RR) is increased in patients with congestive heart failure (CHF), and that the patients with the highest RRs have an increased mortality. The authors hypothesized that CHF patients with the lowest maximum oxygen consumption and the most impaired Weber functional classification would have the highest RR. Eighty-four patients with chronic CHF underwent seated ergometric exercise to exhaustion. Hemodynamic and respiratory gas exchange parameters were measured at rest and peak exercise. Weber functional classifications (A through E) were determined from maximum oxygen consumptions, and patients were stratified to evaluate the RR. The RR increased progressively across Weber classifications at rest (A vs E; P < .001) and with maximum exercise (A vs E; P < .002). At rest, elevation in the RR was related to an increase in the pulmonary pressure gradient (A vs E; P < .002) secondary to increased mean pulmonary arterial pressures. With peak exercise, this elevation was secondary to a decrease in the systemic pressure gradient (A vs E; P < .001). Further analysis revealed that the progressive decrease in the systemic pressure gradient was due to progressively lower mean arterial pressures (A vs E; P < .001). Elevation of the RR, both at rest and peak exercise, predicts a more impaired exercise functional status in patients with chronic CHF. Increases in the RR at peak exercise were related to decreases in mean arterial pressure, most likely limiting perfusion to exercising skeletal muscle. The mechanism of poor exercise blood pressure response in these patients is unclear. Possible explanations include abnormal systemic baroreceptor function with inappropriate vascular adaptation, and a poor cardiac output response to a relative increase in right ventricular afterload in systemic vasodilation seen with exercise.

Adult↗

[Prognosis in patients with myocardial infarction and angiographically normal coronaries].

From a survey on 8,000 coronary angiographic studies performed in our Institute between January 1980 and June 1990, 105 patients were identified as having angiographically normal coronary arteries and myocardial infarction (MI). Coronary arteries considered as normal were subdivided in completely normal (Group I), or slightly abnormal, with minimal lesions resulting in less than 30% narrowing of a major artery, defined as mild coronarosclerosis (Group II). Thirty-five patients were excluded from the study, because of the lack of complete follow-up data; the remaining 70 patients represent the study group we examined. The following parameters were examined: sex, age at the time of acute MI, family of ischemic heart disease, hypertension, dyslipidemia, diabetes, smoking, stable or unstable angina before MI, location of the MI, ejection fraction (EF), presence of completely normal coronary arteries or mild coronarosclerosis. Follow-up was obtained by contacting the patients or their families; post infarction angina, reinfarction, sudden death or cardiac death were noted. The subjects were divided in 2 groups, according to the coronary anatomy; Group I consisted of 41 patients with completely normal coronary arteries and Group II consisted of 29 patients with mild coronarosclerosis. No significant statistical difference was noted between the 2 groups regarding age, sex and coronary risk factors (except for dyslipidemia which was significantly more prevalent in the subjects with mild coronarosclerosis). Prevalence of left ventricular impairment (EF < 45%) and coronary events (angina, reinfarction and death) were significantly higher in Group II. There was no significant difference in age or clinical risk factor prevalence between patients with complicated and non complicated clinical course.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Acute and chronic effects of the dihydropyridine calcium antagonist nisoldipine on the resting and exercise hemodynamics, neurohumoral parameters, and functional capacity of patients with chronic heart failure.

The acute and chronic effects of the dihydropyridine calcium antagonist nisoldipine were studied in patients with chronic heart failure (LV EF < .35; peak VO2 < 25 ml/kg/min) caused by idiopathic or postinfarction cardiomyopathy. The study group initially consisted of 16 patients; two patients were excluded from the acute study due to side effects of the drug and two more patients were excluded during the chronic part of the study because of excessive tachycardia or worsening heart failure, respectively; therefore, the final study group consisted of 12 patients. Each patient was evaluated at rest, in the supine and sitting positions, and during maximal bicycle exercise, before and after acute and chronic (2-3 months) oral nisoldipine therapy (20 mg bid). Plasma levels of renin activity, aldosterone, norepinephrine, and epinephrine were measured before and 1 hour after nisoldipine in 10 patients. Concomitant therapy with digitalis and diuretics was kept constant throughout the study. At rest, in the supine position, nisoldipine (20 mg orally) induced an acute increase of cardiac index from 2.87 +/- 0.52 to 3.93 +/- 1.52 l/min/m2, with a reduction of mean arterial pressure from 97 +/- 7 to 85 +/- 9 mmHg and systemic vascular resistance from 1417 +/- 201 to 968 +/- 257 dynes sec/sec cm5 without significant changes of right atrial and pulmonary pressures. Hemodynamic effects peaked 1 hour after its administration and persisted for 6 hours. Similar changes were observed in the resting sitting position.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Dynamic cardiomyoplasty as an effective therapy for dilated cardiomyopathy.

Nine male patients with dilated cardiomyopathy unresponsive to maximal medical therapy were submitted to dynamic cardiomyoplasty according to the technique described by Carpentier and Chachques, and preliminary postoperative results are reported. Seven patients were in New York Heart Association (NYHA) Class III and two were in intermittent Class IV. The mean age was 56 years (range 51 to 61 years). Preoperative ejection fraction (EF) by multiple gated acquisition ranged from 14% to 28% (mean 20.7%). No additional surgery was performed. Transesophageal echocardiographic monitoring was used during surgery to guide the wrapping procedure. There was no operative mortality. There was one early death (1 month). One late death (sudden death) occurred 7 months after surgery despite significant clinical improvement. Follow-up ranges from 2 to 16 months. Six patients were submitted to hemodynamic evaluation from 4 to 6 months after surgery by transthoracic and transesophageal echo-Doppler assessment. Effective latissimus dorsi support was clearly documented in all patients by comparing postoperative basal hemodynamic values (Cardiomyostimulator [Medtronic, Inc.] switched off) and data obtained during assisted beats (EF increased from 19.4% +/- 8.6% to 32.6% +/- 13.8%, p = 0.043; and stroke volume increased from 51.6 +/- 20.6 mL to 63.0 +/- 22.0 mL, p = 0.014). All patients who completed the latissimus dorsi training protocol were in NYHA Class I or II. A significant reduction in postoperative medical therapy was achieved in all patients. Our preliminary results confirm that the cardiomyoplasty procedure is to be considered a safe and valuable mean for treating selected patients with dilated cardiomyopathy refractory to maximal pharmacological treatment.

Assisted Circulation↗

[Stress and ischemic heart disease].

The role of mental stress in ischemic heart disease is two-fold: as a risk factor of coronary artery disease and as a trigger of acute ischemic attacks in patients with established coronary atherosclerosis. The role of stress as a risk factor is still controversial. Data regarding the relationship between occupational factors and development of coronary atherosclerosis have not been confirmed. A type personality, above all when anger and hostility traits are present, seems to be a predisposing factor for the development of coronary artery disease. These data however, were not confirmed in study groups including patients with a higher prevalence of other, more important, risk factors. Stress can have an important role as a trigger of acute ischemic attacks. This is indirectly shown by the circadian distribution of the main manifestations of ischemic heart disease (sudden death, myocardial infarct, ST segment depression). In fact, their incidence is significantly higher in the morning hours, after awakening, when mental stress is higher. In the laboratory setting, mental stress can induce myocardial ischemia in a variable percentage of patients (0 to 80%). Prevalence of mental stress-induced myocardial ischemia varies depending on the stressor used, the patients group and, above all, the diagnostic tool. Ischemic episodes induced by mental stress, in fact, are generally silent and less severe and extensive than those elicited by exercise stress testing. It is therefore often necessary to use methods, such as myocardial scintigraphy, with higher sensitivity for the detection of myocardial ischemia in comparison with ECG. Patients with mental stress-induced myocardial ischemia tend to present higher scores on measures of aggressivity, anger and hostility. These psychological features are related to a hightened cardiovascular reactivity with a brisk and greater increase in heart rate and blood pressure after exposure to stress. It would be therefore useful to identify patients with such a behaviour by psychological assessment and/or analysis of sympatho-vagal balance by analysis of heart rate variability. The mechanism by which mental stress can induce myocardial ischemia is represented by an increase in myocardial oxygen demand, through the increased heart rate and blood pressure, probably associated with an increase in coronary vascular resistance. This last phenomenon is likely caused by small coronary vessel constriction mediated by alpha-adrenergic activation and by a reduced EDRF release by the damaged endothelium.

Acute Disease↗

[Neurohormonal assessment in heart failure: from the sophisticated laboratory to practical indications].

Heart failure is a syndrome characterized by the activation of neurohumoral mechanisms (sympathoadrenergic, renin-angiotensin, vasopressin) which cause peripheral vasoconstriction, sodium retention and myocardial hypertrophy. In acute myocardial disfunction these systems can play a critical role in patient survival, however, they can directly worsen myocardial function and patient prognosis on a long-term basis. Other neurohumoral systems activated in heart failure (atrial natriuretic factor, prostaglandins, dopamine) tend to counterbalance the vasoconstrictive, sodium retentive mechanisms. Though their secretion is increased in heart failure, it is however not sufficient, and peripheral vasoconstriction and sodium retention prevail. Moreover the role of local factors, such as tissue renin-angiotensin system, EDRF and endothelin secretion has been recently pointed out. Neurohumoral activation is directly related to the severity of the clinical and hemodynamic impairment and prognosis of the patient with heart failure. A thorough evaluation of the neurohumoral mechanisms is therefore of paramount importance for the assessment of patients with heart failure. Neurohumoral activation can be roughly assessed using some simple laboratory measurements: plasma sodium concentration, for example, is inversely related to the degree of activation of many neurohormones such as norepinephrine, angiotensin II, vasopressin and atrial natriuretic factor. The method most commonly used to assess neurohumoral activity relies on the direct measurement of the plasma concentrations. It must be noted, however, that plasma levels are critically dependent on many factors besides hormone secretion and metabolism. For example, 3-4 days on a low sodium diet or standing for at least 2 hours can increase plasma renin activity in a normal subject from 1.5 to 5-10 pg/ml/hr. Plasma concentrations of neurohormones are related to the factors controlling their secretion: for example, "normal" values of plasma renin activity in presence of fluid retention and edema are to be judged as excessively elevated. Autonomic nervous system activity can also be assessed studying reflexes in which this system is involved (orthostasis, cold pressor test, phenylephrine test...). Another method consists in the study of the spontaneous variability of some parameters controlled by this system, such as heart rate and blood pressure. The most reliable method is based on the power spectral analysis of heart rate variability. With this last method, a low frequency component depending mainly on sympathetic activity and an high frequency component depending on vagal activity can be identified in heart rate variability. Thus, complex phenomena such as sympatho-vagal balance can be easily studied through simple noninvasive tools.

Adrenal Glands↗

Exercise hyperventilation chronic congestive heart failure, and its relation to functional capacity and hemodynamics.

The ventilatory response to exercise was evaluated in 26 normal sedentary men and 68 patients with chronic heart failure using the slope of the relation between minute ventilation (VE) and carbon dioxide production (VCO2). All subjects underwent maximal upright bicycle cardiopulmonary exercise testing; 33 patients also underwent right-sided cardiac catheterization. The slope of VE/VCO2 was calculated by linear regression analysis using data from all the exercise tests and the first 60% of exercise duration; a high correlation was seen between these results (r = 0.83; p less than 0.001). The slope of VE/VCO2 was significantly, though weakly, related to peak exercise work load, oxygen consumption and ventilatory threshold (r = -0.49, -0.56 and -0.49, respectively), several peak exercise hemodynamic parameters and peak exercise dead space/tidal volume ratio (r = 0.70). With use of multivariate analysis, the only independent determinants of the slope were peak exercise dead space/tidal volume ratio and cardiac index. Thus, in patients with heart failure, exercise hyperventilation can contribute to the impairment of functional capacity and can be considered a compensatory response to abnormal hemodynamics and lung blood distribution in order to keep blood gas concentrations normal.

Cardiac Catheterization↗

Effects of acute and chronic ibopamine administration on resting and exercise hemodynamics, plasma catecholamines and functional capacity of patients with chronic congestive heart failure.

The effects of acute and chronic ibopamine treatment on resting and exercise hemodynamics, exercise capacity and plasma catecholamines were evaluated in 25 patients with chronic heart failure, using a double-blind, parallel, placebo-controlled design. During 2 months of therapy with either placebo or ibopamine (100 mg, 3 times daily), 1 patient was withdrawn from each group for worsening heart failure, New York Heart Association functional class improved in 4 patients on ibopamine and in 1 on placebo, and furosemide dose could be decreased in 4 on ibopamine and in no patient on placebo. Acute ibopamine administration induced, in comparison with placebo, a significant increase of cardiac and stroke volume indexes both at rest and peak exercise, with a reduction of systemic vascular resistance. These hemodynamic changes were maintained also after chronic therapy, with no evidence of tolerance development. Exercise capacity (evaluated as peak exercise duration and oxygen consumption, and ventilatory threshold) did not significantly change. Resting and peak exercise norepinephrine plasma levels were significantly reduced after both acute and chronic ibopamine administration. Thus, the hemodynamic and neurohumoral effects of ibopamine make this drug potentially useful for the chronic treatment of congestive heart failure.

Deoxyepinephrine↗