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Biomedical subjects

M Guazzi

Publications and source records attributed to M Guazzi.

At least 91 records · Page 5Linked to original sources
PubMed1992

[Interrelation of plasma volume, fluid metabolism and neurohormonal activation after ultrafiltration in congestive heart failure].

Ultrafiltration improves the clinical condition of patients with congestive heart failure (CHF) through a reduction of excessive body water. We investigated the relationships among intra and extravascular fluids, hemodynamics and neurohumoral pattern following plasma water subtraction. In 55 patients with CHF (35 in NYHA class IV, Group A, and 20 in NYHA class II-III, Group B), removal of 3242 +/- 201 ml and 1741 +/- 119 ml of plasma water acutely reduced plasma volume (calculated from hematocrit changes) by -20.7% and -12.9% in Group A and in Group B, respectively. Plasma volume returned to baseline values within 48 hours. Body weight and ventricular filling pressures also lowered and remained so for 2 days. After ultrafiltration urinary output increased and norepinephrine, renin activity and aldosterone plasma levels decreased in Group A, while a fall of diuresis and a rapid rise of plasma levels of the 3 hormones were observed in Group B. Two days after ultrafiltration the persistence of reduced body weight with recovery of plasma volume indicates a shift of fluid from the extravascular to the intravascular compartment. The different behaviour of hemodynamics, urinary output and neurohumoral pattern changes observed in the 2 groups after ultrafiltration, suggest that in severe heart failure (Group A) the physiological responses to intravascular volume depletion are unsettled while are preserved in less severe stages of the disease (Group B).

Adult↗
PubMed1991

Usefulness of excitable gap and pattern of resetting in atrial flutter for determining reentry circuit location.

Clinical and experimental data show that type I atrial flutter is due to a reentry mechanism with an excitable gap. To define the location of the reentry circuit of atrial flutter, width of excitable gap, poststimulation cycle and pattern of reset after premature stimulus were analyzed in 18 patients during atrial flutter at multiple atrial sites (high, lateral, posterior and septal right atrium, and coronary sinus). The pattern of reset was defined as flat or increasing whether the return cycle remained unchanged or prolonged with increasing prematurity. Shorter values of the excitable gap were found at the coronary sinus (33 +/- 8 ms) and high right atrium (30 +/- 10 ms) than at the posterior (43 +/- 9 ms) or septal right atrium (45 +/- 11 ms). Intermediate values (36 +/- 8 ms) were measured at the lateral right atrium. Poststimulation cycle, corrected for atrial flutter cycle length, was shorter in the posterior (6 +/- 7 ms) and septal right atrium (5 +/- 7 ms) than in the coronary sinus (35 +/- 9 ms), and the high (23 +/- 10 ms) and lateral right atrium (15 +/- 9 ms). A flat pattern of resetting occurred more frequently at the septal (18 of 18 patients) and posterior right atrium (15 of 18) than at the lateral (8 of 18) and high right atrium (2 of 17), and was never observed at the coronary sinus. Atrial flutter was successfully terminated by overdrive atrial pacing in 15 of 18 patients, and termination was more easily obtained from the septal and posterior right atrium.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Flutter↗
PubMed1991

Upward shift of the lower range of coronary flow autoregulation in hypertensive patients with hypertrophy of the left ventricle.

BACKGROUND: At any given perfusion pressure, coronary reserve is expressed by the difference between autoregulated and maximally vasodilated flow. In hypertension the raised coronary resistance reduces the steepness of the pressure-flow relationship at maximal vasodilatation. In the presence of cardiac hypertrophy the line of autoregulated flow becomes higher. For these reasons coronary reserve is reduced and the point at which baseline flow approaches the maximal achievable flow might be shifted to a higher perfusion pressure. Thus, any reduction below this elevated and critical value of pressure would lower the coronary flow. METHODS AND RESULTS: The investigated patients were normotensive (controls, nine) and hypertensive with normal (group I, seven) or augmented LV mass index because of concentric LV hypertrophy (group II, eight). All had effort-induced angina and angiographically normal left epicardial branches. Flow in the great cardiac vein was measured by thermodilution in the baseline and during stepwise (5 mm Hg every 5 minutes) decrease of the coronary perfusion pressure with a titrated nitroprusside i.v. infusion; perfusion pressures of 60 mm Hg in the controls and 70 mm Hg in the hypertensives were taken as end points. Baseline flow averaged 102 ml/min in normotensives, 104 ml/min in hypertensive group I and 148 ml/min in hypertensive group II. At the end points flow was similar to baseline in the controls and group I. In group II coronary flow started to decline and myocardial O2 extraction started to slightly but significantly rise at perfusion pressures of 90-80 mm Hg; at the end point flow was reduced by 26% (p less than 0.01 from baseline). The perfusion patterns did not seem to be related to the changes in tension-time index and heart rate. CONCLUSIONS: The association of high blood pressure (reduced ability of the coronary arterioles to dilate) and hypertrophy of the myocardium (augmented baseline coronary flow) may shift the point of exhaustion of coronary reserve to a higher perfusion pressure and make the myocardium vulnerable to treatment-induced relative hypertension.

Blood Pressure↗
PubMed1991

Angiographic evolution of coronary atherosclerosis in patients receiving propranolol. A two-year follow-up.

STUDY OBJECTIVE: To test whether propranolol may influence the progression of coronary atherosclerosis. DESIGN: Repeat coronary angiography after two year treatment and evaluation of changes in coronary narrowings. SETTING: Subjects with effort angina of recent onset requiring coronary angiography and medical treatment. PATIENTS: 80 untreated patients, with a greater than or equal to 50 percent focal narrowing on a major coronary branch associated or not with a less than 50 percent stenosis of other major branches. They were randomized to isosorbide dinitrate (40 mg bid) (group 1, control group) or to propranolol (80 mg qid) (group 2, treatment group). RESULTS: At restudy, there were more diseased vessels and These narrowings per patient in both groups. Multivessel involvement and greater than or equal to 50 percent obstructions were also augmented. These changes were not statistically significant. Patients with progression of the stenotic tracts (both greater than or equal to 50 percent and less than 50 percent were 19 (48 percent) in group 1 and 28 (70 percent) in group 2 (p less than 0.05). Narrowings with progression were 25 in group 1 and 48 in group 2. Thirteen narrowings in group 1 and 15 in group 2 were newly detected at restudy. Eighteen patients (45 percent) in group 1 and nine (23 percent) in group 2 had a steady disease. Smoking, high blood pressure, family history of coronary disease, blood glucose values and lipid levels were considered; the only significant group differences were 31 percent rise of total triglyceride and 23 percent decrease of HDL cholesterol in patients who were treated with propranolol. CONCLUSIONS: Propranolol showed an adverse influence on coronary atherosclerosis, regarding the evolution of both greater than or equal to 50 percent and less than 50 percent narrowings and not the formation of new stenoses. Changes in serum lipid values might have a role.

Angina Pectoris↗
PubMed1991

[The excitatory effect of adenosine on the discharge activity of the afferent cardiac sympathetic fibers].

Recent clinical observations suggest that adenosine may produce cardiac pain; even though the mechanisms involved still need defining, one of the most convincing hypotheses seems to be a direct adenosine stimulation of the sympathetic nerve endings present in the myocardium. In 10 decerebrate and artificially ventilated cats, single sympathetic afferent fibres innervating the left ventricle were isolated from the third white thoracic ramus communicans of the left sympathetic chain. After locations of the fibre receptor field on the cardiac surface, we evaluated the effects of the local epicardial application of adenosine (0.1, 1 and 10 mg/ml) on the nervous discharge activity. These results were compared with those obtained by application of bradykinin, a potent natural algogenic substance which activates sympathetic afferents, and by a mechanical stimulus such as a slight increase of systolic arterial pressure (46 +/- 6% from 113 +/- 18 mmHg) induced by partial occlusion of the thoracic aorta. In particular, adenosine (1 mg/ml) elicited a significant increase in impulse activity (from 0.11 +/- 0.02 to 0.36 +/- 0.06 imp/0.1 s) with a latency of 16 +/- 2 s. Bradykinin application (20 micrograms/ml), in the same way, produced a significant increase in impulse activity (from 0.11 +/- 0.01 to 0.86 +/- 0.16 imp/0.1 s) with a latency of 8 +/- 1 s. Neither situation showed significant hemodynamic changes. An increased neural discharge (from 0.11 +/- 0.02 to 0.26 +/- 0.04 imp/0.1 s) was also observed during aortic occlusion. After purinergic receptor blockade by aminophylline (5 mg/kg, iv), the response to adenosine was no longer observed, while responses to bradykinin and aortic occlusion were unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1991

[The surgical treatment of pre-excitation syndromes].

In the recent years the approach to the patients with tachycardias due to the Wolff-Parkinson-White (WPW) syndrome has changed in relation to the favourable results obtained by the surgical treatment. In this review the significance of the pre-operative electrophysiologic study is analyzed, as to a guide to localize the accessory pathway and, in particular, to disclose the presence of complicated substrates, such as multiple accessory pathways, AV nodal reentry; these latter situations if not correctly diagnosed, are a cause of surgical failure. We report the use of the epicardial surgical approach (Guiraudon technique). With the recent modifications, this technique avoids in the most cases the use of extracorporeal circulation. This simplified and safe surgical technique is a suitable alternative to other therapeutic strategies.

Electrocardiography↗
PubMed1990

Changes in circulating norepinephrine with hemofiltration in advanced congestive heart failure.

In congestive heart failure (CHF), hemofiltration is associated with an obvious decrease in circulating norepinephrine. This method was used for investigating the mechanisms whereby plasma norepinephrine is increased in chronic CHF. In 23 cases of advanced CHF, hemofiltration (2,983 +/- 1,228 ml) lowered plasma norepinephrine by 515 +/- 444 pg/ml. This effect was prompt, persisted or became greater in the next 24 hours. It was not associated with significant changes in cardiac output, aortic pressure or systemic vascular resistance. It did not appear to depend on variations in parameters related to the sympathetic activity, such as plasma renin, right atrial, wedge pulmonary artery and renal perfusion pressures, and was independent of duration and amount of hemofiltration. These observations did not support the concept that the norepinephrine decrease was the main consequence of a neural sympathetic inhibition. Hemofiltration increased diuresis by 606 +/- 415 ml; changes were prompt and correlated inversely (r = -0.7; p less than 0.01) with those in plasma norepinephrine. The same unknown mechanism of the increased urinary output might potentiate the norepinephrine removal from the blood by the kidney, or hemofiltration and the augmented diuresis might result in a regression of congestion of lungs and kidneys, leading to an improved extraction of norepinephrine. In CHF, a relation may exist between fluid retention and norepinephrine and in advanced stages, circulating norepinephrine, although strikingly increased, is devoid of important cardiovascular effects. At these stages, plasma norepinephrine is probably unreliable as an index of the sympathetic neural activity.

Adult↗
PubMed1990

[The right ventricle and pulmonary circulation in hypertensive patients].

Elevated blood pressure and vascular resistance in patients with systemic hypertension are paralleled by a proportional rise in pressure and resistance in the lesser circulation. It was hypothesized that increased systemic reaction to adrenergic stimulation is shared by the pulmonary vessels. Thus normotensive subjects and patients with primary hypertension were investigated during mental arithmetic and the cold pressor test. Both groups responded to both stimuli; during arithmetic pressure reaction was mediated through an increase of cardiac output, and during the cold pressor test through a predominant rise in systemic vascular resistance. The pressure changes were emphasized in the hypertensive population. Pressure in the pulmonary artery in normotensive subjects was not affected by cold and was slightly raised (systolic) during arithmetic. In hypertensive patients, on the other hand, systolic and diastolic pressures were consistently augmented by both tests, and pulmonary arteriolar resistance rose by 42% and 29% of control during the cold pressor test and arithmetic, respectively. Changes in resistance reflected neurally-mediated vasoconstriction but not variations in the passive relationship between pressure and flow, since during arithmetic, for a similar rise in flow the driving pressure across the lungs was steady in normotensive subjects and rose significantly in hypertensive patients. In these same patients pressure was augmented by cold test in the absence of substantial changes in flow. At baseline and during tests pulmonary wedge pressure, pleural pressure, arterial blood gases, and pH were similar in the two populations. The intravenous infusion of similar scalar doses of norepinephrine (the same mediator released during cold test) was not effective on the pulmonary vessels of normotensives and caused an obvious vasoconstriction in hypertensives.(ABSTRACT TRUNCATED AT 250 WORDS)

Catecholamines↗
PubMed1989

[Multicenter, double-blind study comparing rilmenidine 1 mg and hydrochlorothiazide 25 mg in 244 patients].

The efficacy and acceptability of Rilmenidine (RIL) were assessed in a multicentre, controlled, double-blind trial versus hydrochlorothiazide (HCZ) in patients with mild to moderate hypertension. After an initial 4 week washout period on placebo, patients with diastolic BP of between 90 and 110 mmHg were administered in monotherapy either RIL 1 mg or HCZ 25 mg for four weeks (Day 0-Day 28). In the following four weeks (Day 28-Day 56), those with diastolic BP of over 90 mmHg were given, in association, the antihypertensive agent that they had not received initially. The other patients continued the trial with single daily doses of monotherapy. Two hundred and fourty four patients (48.4 +/- 0.6 years) with supine systolic and diastolic BP of 155.86 +/- 0.96 mmHg and 101.02 +/- 0.28 mmHg respectively were randomly allocated to two comparable treatment groups (RIL, n = 120 and HCZ, n = 124). The systolic and diastolic BP decreased significantly between Day 0 and Day 28, as much at Day 14 as at Day 28 in both treatment groups. The antihypertensive effect was comparable: at Day 28 the mean fall in systolic/diastolic BP was 16/10 mmHg in the RIL group and 15/9 mmHg in the HCZ group (NS). The clinical acceptability was equivalent in the two groups: secondary effects were responsible for one patient's withdrawal in each group and their incidence was 5% on average, 10% for the most common.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1989

[Angiographic course of coronary atherosclerosis in angina pectoris. Its relation to 2 years' treatment with propranolol, nifedipine and nitrates].

Calcium antagonists and beta-blockers may retard or inhibit atherogenesis. We tested whether nifedipine or propranolol may retard or induce regression of coronary atherosclerosis in man. In selected population of 113 patients with effort angina and proven coronary artery disease, the coronary cineangiographic pattern after 2 year therapy with nifedipine (Group 1, 39 patients), propranolol (Group 2, 36 patients), or isosorbide dinitrate (control group, 38 patients) was compared to the pre-treatment pattern. After 2 years the disease evolved to a different extent in the 3 groups. The number of lesions with evidence of progression was significantly smaller after nifedipine (14), and larger after propranolol (39) as compared with controls (24). Patients with evidence of progression of old lesions, and appearance of new lesions were significantly fewer in Group 1 than in Group 2 and in control patients. Thus, nifedipine seemed more protective than either of the other drugs against coronary atherosclerosis. The coronary risk factors were within normal limits in the nifedipine treated group and remained so with treatment supporting that they were likely dissociated from influences on atherosclerosis. The evolution, at least as judged by the number of lesions with progression, appeared significantly (p less than 0.01) worse with propranolol than with isosorbide dinitrate. This may prospect that nitrate contrasted the evolution of the disease, or that propranolol made it worse, possibly through unfavourable modifications of serum lipids (28% rise of total triglyceride and 25% decrease of HDL cholesterol were already detectable at 12 months in Group 2).

Adult↗