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Biomedical subjects

M D Guazzi

Publications and source records attributed to M D Guazzi.

At least 19 recordsLinked to original sources
PubMed2000

How the left and right sides of the heart, as well as pulmonary venous drainage, adapt to an increasing degree of head-up tilting in hypertrophic cardiomyopathy: differences from the normal heart.

OBJECTIVES: We aimed to assess the differences in the adaptive response of patients with hypertrophic cardiomyopathy (HCM) compared with normal subjects, as well as any association with increased susceptibility to the test. BACKGROUND: Diastolic function contributes importantly in the adaptation of the normal heart to head-up tilting. This mechanism may be disturbed by an impaired relaxation in HCM. METHODS: Twenty-one male patients with HCM (46 +/- 6 years old) and 22 healthy men (44 +/- 8 years) were studied using Doppler echocardiography after 1 and 10 min of head-up tilting at 20 degrees, 40 degrees and 60 degrees. RESULTS: In control subjects, tilting was associated with 1) a predominance of diastolic pulmonary venous flow and early left ventricular (LV) filling (atrium functioning as an open conduit); 2) right ventricular (RV) shrinkage; and 3) no LV dimensional variations. In patients with HCM, tilting was associated with 1) a prevalence of systolic pulmonary venous flow (atrium functioning as a reservoir in which filling depends on atrial relaxation and compliance) and late diastolic transmitral flow (atrium working as a booster pump); 2) LV shrinkage; and 3) no RV dimension variations. These mechanisms did not prevent stroke volume (SV) from decreasing at 40 degrees and 60 degrees in both groups. Because of a lower increase in heart rate (HR), a reduction in cardiac output (CO) was greater in patients with HCM. The responses were similar after 1 and 10 min of tilting in control subjects, whereas in patients, blood pressure (BP), SV and LV dimension fell more after 10 min. CONCLUSIONS: Adaptation of the normal heart to tilting is based on a ventricular interaction and LV diastolic properties; HCM relies on left atrial diastolic and systolic functions. An inadequate HR reaction to a fall in BP and SV in HCM (depressed reflexogenic activity) contributes to making CO more vulnerable by greater and more prolonged displacements.

Adaptation, Physiological↗
PubMed1999

Exercise-induced hemoconcentration in heart failure due to dilated cardiomyopathy.

Exercise-induced hemoconcentration is a useful mechanism, particularly in heart failure, because it increases oxygen content of blood, perfusing the working muscles; in 50 normal subjects and 50 patients with congestive heart failure, hemoglobin at peak exercise increased by 7 +/- 3% and 5 +/- 3%, respectively. Hemoconcentration was due to fluid flux out of the vascular bed, likely through oncotic forces related to intracellular lactate accumulation and not to red blood cell recruitment from other organs (spleen), because hemoglobin increase, as a percentage, was similar to plasma protein increase.

Adult↗
PubMed1999

Pulmonary function, cardiac function, and exercise capacity in a follow-up of patients with congestive heart failure treated with carvedilol.

BACKGROUND: Chronic heart failure causes disturbances in ventilation and pulmonary gas transfer that participate in limiting peak exercise oxygen uptake (VO(2p )). The beta-adrenergic receptor blocker carvedilol improves left ventricular (LV) function and not VO(2p). This study was aimed at investigating the pulmonary response to changes in LV performance produced by carvedilol in patients with chronic heart failure. METHODS: Twenty-one patients with New York Heart Association class II to III heart failure were randomly assigned (2 to 1) to carvedilol (25 mg twice daily, n = 14) or placebo (n = 7) for 6 months. Rest forced expiratory volume (FEV(1)), vital capacity, total lung capacity, carbon monoxide diffusing capacity, its alveolar-capillary membrane component, pulmonary venous and transmitral flows (for monitoring changes in LV end-diastolic pressure), LV diastolic and systolic dimensions, stroke volume, ejection fraction, and fiber shortening velocity were measured at baseline and at 3 and 6 months. VO(2p), peak ratio of dead space to tidal volume (VD/VT(p)), ventilatory equivalent for carbon dioxide production (VE/VCO(2)), and VO(2) at anaerobic threshold (VO(2at)) were also determined. RESULTS: FEV(1), vital capacity, total lung capacity, carbon monoxide diffusing capacity, and the alveolar-capillary membrane component were impaired in chronic heart failure compared with 14 volunteers and did not vary with treatment. Carvedilol reduced end-diastolic pressure, end-diastolic diameter, and end-systolic diameter and increased ejection fraction, stroke volume, and fiber shortening velocity without affecting VO(2p), VO(2at), VD/VT(p), or VE/VCO(2) at 3 and 6 months. Placebo did not produce significant changes. CONCLUSIONS: In chronic heart failure carvedilol ameliorates LV function at rest and does not significantly affect ventilation and pulmonary gas transfer or functional capacity. These results suggest that improvement in cardiac hemodynamics with carvedilol does not reverse pulmonary dysfunction. Persistent lung impairment might have some role in the failure of carvedilol to improve exercise performance.

Adrenergic beta-Antagonists↗
PubMed1999

Impeded alveolar-capillary gas transfer with saline infusion in heart failure.

The microvascular pulmonary endothelium barrier is critical in preventing interstitial fluid overflow and deterioration in gas diffusion. The role of endothelium in transporting small solutes in pathological conditions, such as congestive heart failure (CHF), has not been studied. Monitoring of pulmonary gas transfer during saline infusion in CHF was used to probe this issue. Carbon monoxide diffusion (DL(CO)), its membrane diffusion (D(M)) and capillary blood volume (V(C)) subcomponents, and mean right atrial (rap) and mean pulmonary wedge (wpp) pressures after saline or 5% D-glucose solution infusions were compared with baseline in 26 moderate CHF patients. Saline was also tested in 13 healthy controls. In patients, 750 mL of saline lowered DL(CO) (-8%, P<0.01 versus baseline), D(M) (-10%, P<0.01 versus baseline), aldosterone (-29%, P<0.01 versus baseline), renin (-52%, P<0.01 versus baseline), and hematocrit (-6%, P<0.05 versus baseline) and increased V(C) (20%, P<0.01 versus baseline), without changing rap and wpp. Saline at 150 mL produced qualitatively similar results regarding DL(CO) (-5%, P<0.01 versus baseline), D(M) (-7%, P<0.01 versus baseline), V(C) (9%, P<0.01 versus baseline), rap, wpp, aldosterone (-9%, P<0.05 versus baseline), and renin (-14%, P<0.05 versus baseline). Glucose solution (750 mL), on the contrary, increased DL(CO) (5%, P<0.01 versus 750 mL of saline) and D(M) (11%, P<0.01 versus 750 mL of saline) and decreased V(C) (-9, P<0.01 versus 750 mL of saline); aldosterone (-40%), renin (-41%), hematocrit (-3%), rap, and wpp behaved as they did after saline infusion. In controls, responses to both saline amounts were similar to responses in CHF patients regarding aldosterone, renin, hematocrit, rap, and wpp, whereas DL(CO), D(M), and V(C) values tended to rise. Hindrance to gas transfer (reduced DL(CO) and D(M)) with salt infusion in CHF, despite an increase in V(C) and no variations in pulmonary hydrostatic forces, indicates an upregulation in sodium transport from blood to interstitium with interstitial edema. Redistribution of blood from the lungs, facilitating interstitial fluid reabsorption, or sodium uptake from the alveolar lumen by the sodium-glucose cotransport system might underlie the improved alveolar-capillary conductance with glucose.

Aldosterone↗
PubMed1998

Thrombin activation and late restenosis after percutaneous transluminal coronary angioplasty.

BACKGROUND: Mechanisms of restenosis after percutaneous transluminal coronary angioplasty (PTCA) have not been defined yet. Experimental studies have shown that thrombin, by stimulating platelet growth factor secretion and smooth muscle cell proliferation, can play a major role. METHODS AND RESULTS: In 34 patients with single-vessel coronary disease undergoing PTCA, thrombin activity was evaluated through serial fibrinopeptide A (FPA) plasma determinations. Samples were performed before PTCA, immediately after and 24 hours, 72 hours, and 6 months later. Patients were grouped according to the development (group 1, n = 13) or nondevelopment (group 2, n = 21 ) of restenosis at a 6-month angiographic control. No difference in the two groups was found concerning baseline FPA values. In patients in group 1, soon after PTCA higher FPA levels (27.3 +/- 13.7 ng/ml) than those in group 2 (9.2 +/- 5.6 ng/ml; p < 0.05 vs pre-PTCA, and p < 0.01 between the two groups) were observed. No differences in FPA levels were detected at the other steps between the two groups. CONCLUSION: Our data suggest that thrombin plays a role in the process of restenosis after PTCA; acute FPA response to the procedure seems to have a predictive value.

Aged↗
PubMed1998

Antihypertensive efficacy of angiotensin converting enzyme inhibition and aspirin counteraction.

OBJECTIVE: Blockade of bradykinin breakdown and enhancement of prostaglandin release probably participate in the antihypertensive activity of angiotensin converting enzyme (ACE) inhibitors. Cyclooxygenase blockers may attenuate the efficacy of ACE inhibitors by interfering with prostaglandin synthesis, and patients taking aspirin may not benefit from ACE inhibition. This study was designed to evaluate the incidence of the counteractive phenomenon and to define minimal aspirin dosage that causes an antagonistic effect. METHODS: These were 26 patients with mild to moderate hypertension (group 1) and 26 patients with severe untreated primary hypertension (group 2). Enalapril (20 mg twice a day) was used as a single drug in group 1 and was added to the combination of long-acting nifedipine (30 mg/day) and atenolol (50 mg/day) in group 2. Aspirin was tested at doses of 100 and 300 mg/day, and an attenuation of more than 20% of the mean blood pressure decrease produced by enalapril was the criteria that defined antagonism. RESULTS: The 100 mg dose was ineffective. However, 300 mg aspirin had an antagonistic effect in 57% of patients in group 1 and 50% of patients in group 2: mean arterial pressure was lowered by 63% and 91% less, respectively. Results were independent of the drug administration order. In "responders," aspirin significantly attenuated the renin rise associated with ACE inhibition. CONCLUSIONS: These findings suggest that a number of ACE-inhibited patients are susceptible to 300 mg/day aspirin, regardless of hypertension severity. Antagonism may be mediated through prostaglandin inhibition according to predominance, in an individual patient, of prostaglandin activation (also as a renin secretory stimulus) or angiotensin blockade by enalapril.

Adult↗
PubMed1998

[Early evaluation of results from systemic thrombolysis in acute myocardial infarct: the value of troponin I].

Cardiac troponin-T (Tn-T) and troponin I (Tn-I) isoforms are sensitive and specific tests for the diagnosis of acute myocardial infarction. Information is scanty regarding the ability of these markers to discriminate patients with or without reperfusion early after thrombolytic treatment. To this purpose, 64 patients (mean age 63.7 +/- 7.5 years) with acute myocardial infarction, treated with recombinant tissue-type plasminogen activator within 6 hours from the onset of symptoms, were enrolled in the study. Tn-I was determined by immunofluorescency (Dade, Stratus II) at the beginning of thrombolysis, 30 min after therapy (120 min after starting) and every 6 hours in the first 2 days of acute myocardial infarction. At the same intervals, samples for Tn-T (immunoenzymatic methods ELISA), creatin phosphokinase (CK) and CK-MB (biochemical method) were collected. Normal subjects showed values of Tn-I and Tn-T steadily lower than 0.2 micrograms/l. To evaluate reperfusion, for each parameter the time to peak concentration and the ratio (delta) between the levels of the marker 30 min after thrombolysis vs basal, were considered. Coronary angiography was performed in all patients within 4 days, in 48 patients (Group 1) reperfusion (TIMI grade 2-3) of the involved vessel was reached, in 16 (Group 2) reperfusion was absent (TIMI 0-1). In Group 1, at 30 min after the end of thrombolysis, an increase of cardiac Tn-1 of at least 5.5 times compared to baseline, was observed; In-T, CK and CK-MB reached concentrations at least 7-fold greater than basal ones; in Group 2 patients, no significant variation of concentration of all markers was found. Therefore, in order to discriminate between reperfused and non reperfused patients, cut-off values of the ratio delta of 5.5 for Tn-I and of 7 for Tn-T were chosen. By this method, sensitivity for detection of reperfusion was 95, 80, 54 and 56%; specifically 100, 89, 79 and 82%, respectively. In Group 1 Tn-I peaked earlier than other parameters (9.2 +/- 1.7 vs 12.4 +/- 2.4 hours for Tn-T, p< 0.04 and vs 13 +/- 1.7 hours for CK and CK-MB, p<0.03); the peak of each marker showed the following values of sensitivity and specificity for reperfusion: 86 and 89% for Tn-I, 79 and 82% for Tn-T, 78 and 80% for CK, 83 and 80% for CK-MB. The time to peak of troponins, CK and CK-MB is a sensitive index of reperfusion after thrombolytic therapy in acute myocardial infarction; the delta Tn-I is the earliest marker of reperfusion allowing the assessment of efficacy of treatment within 2 hours after its beginning.

Adult↗
PubMed1997

Evidence of multifocal activity of coronary disease in patients with acute myocardial infarction.

BACKGROUND: Destabilization of the fibrous cap facilitates plaque rupture, thrombus formation, and myocardial infarction. Because systemic stimuli, such as lipoproteins, infectious agents, and autoantigens, may incite this reaction, one may wonder whether disruption mechanisms are only local or systemic and infarction is caused by an arbitrary plaque event or by a systemic, acute activity of the coronary disease. METHODS AND RESULTS: Early (3 to 5 days) and late (1 month) peri-infarction coronary angiographic data in 23 patients with first infarction were compared with that in 23 similar patients, with angiography performed because of stable angina and repeated after 1 month before angioplasty. Nonculprit lesion changes at the narrowest point defined progression or regression when exceeding 0.27 mm. In patients with recent infarction we found that 16 had progression, 4 had regression, 1 had both, 2 were steady (values in patients with stable angina being 2 [P<.0011, 1 [NS], 0 [NS], and 20 [P<.001]); 27 lesions were infarct related; 17 of the 45 nonculprit lesions progressed and 5 regressed (values in stable angina being 2 [P<.001] and 1 [P<.05] out of 78); minimal diameter reduction of progressing stenoses averaged 0.39 mm; lumen increase of regressing lesions averaged 0.30 mm; 3 patients developed interim rest angina associated with progression of a nonculprit lesion. CONCLUSIONS: A greater proportion of subjects and lesions with progression or regression (in infarction versus stable angina) supports the hypothesis that infarction is a hallmark of systemic coronary disease activity. Changes might vary according to the "maturation" stage of an atheroma, and maximal expression would be at the level of the offending plaque. Shrinkage, thrombolysis, or vascular remodeling would determine the residual plaque morphology.

Analysis of Variance↗
PubMed1996

Reversal of heart failure with sotalol in a case of incessant supraventricular tachycardia.

Supraventricular tachycardia inducing severe left ventricular enlargement and dysfunction was treated with sotalol in a 17-year-old man, in whom radiofrequency ablation had been unsuccessful. Restoration of sinus rhythm overwhelmed the negative inotropic effect of the drug and caused full reversion to normal of the left ventricular dimensions and function.

Adolescent↗