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Biomedical subjects

M D Guazzi

Publications and source records attributed to M D Guazzi.

At least 91 records · Page 5Linked to original sources
PubMed1991

[Changes in pulmonary vascular reactivity to adrenergic stimuli in congestive heart failure].

Heart failure is associated with increased activity of sympathetic nervous system. As to the latter's effector organs, attention has been mainly drawn by heart and systemic circulation. In this study we investigated whether and how the neurogenic vasomotility of the lesser circulation is modified. Therefore, we compared 12 patients with heart failure in III NYHA functional class, with 10 subjects, undergoing hemodynamic study for diagnostic reasons and found to be normal. The neurogenic reactivity of pulmonary vessels was assayed by means of 2 sympathetic stimuli: arithmetic test (AT) and cold pressor test (CPT), performed both with and without obstruction to right heart venous return. This was obtained by expanding a balloon in inferior vena cava, in order to rid the neurogenic component of pulmonary vasomotility of the interference of the normally prevailing mechanical component (consisting in adaptations to flow variations). AT caused pulmonary vasodilation in normal subjects, as a passive consequence of the increase of cardiac output and, therefore, of pulmonary flow. Caval obstruction, by simply restraining this increase, induced a clearly neurogenic vasoconstrictor response. On the contrary, in failing patients, a slight vasodilation, independently from the condition of venous return, was observed. This took place in spite of the constant absence of any variations of cardiac output, which both indicates the reduction of myocardial function and helps to show the diminished nervous influence on pulmonary circulation. On the other hand, CPT had a vasoconstrictor effect in both groups, though potentiated by the reduction of transpulmonary flow in normal subjects only.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
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

Acute coronary vasomotor effects of nifedipine and therapeutic correlates in syndrome X.

In 18 patients (12 women) presenting with effort-induced chest pain and normal coronary angiograms (syndrome X), 10 mg sublingual nifedipine increased the lumen of major coronary arteries (quantitative angiography) by 13 +/- 10% (p less than 0.01), coronary blood flow (thermodilution) by 23 +/- 26% (p less than 0.05), norepinephrine plasma concentration by 60 +/- 42% (p less than 0.01) and decreased the global ST-segment shift during the effort stress test from 8.8 +/- 4.1 to 7 +/- 6.8 mm (p less than 0.03) at comparable maximal workload and at unchanged double product. There was a correlation (positive) of changes in flow with changes in coronary lumen diameter (r = 0.65, p less than 0.01) with ST-segment response to exercise (r = 0.83, p less than 0.001) and with (inverse) norepinephrine plasma concentration (r = -0.70, p less than 0.01); no correlation was found between ST-segment response and changes in arterial lumen diameter. In a few cases, nifedipine did not improve or even worsened the response to exercise; coronary flow was unchanged or decreased and norepinephrine plasma levels were modestly or greatly increased, respectively. After 4 weeks of treatment with nifedipine (10 to 20 mg 4 times daily), the effort ST-segment shift was further decreased to 4.4 +/- 3.5 mm (p less than 0.03) despite a slightly increased double product. Plasma norepinephrine values, as compared to those after acute nifedipine, were decreased by 40% in patients with further improvement and were unchanged in patients whose exercise performance did not vary.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Sublingual↗
PubMed1990

[Coronary vasomotor equivalents in the electrocardiographic behavior in induced ischemia].

In effort angina the exercise test can shift the ST-segment during the active phase and/or recovery. To investigate whether coronary vasomotility has some part in these electrocardiographic patterns, in 15 patients with stable effort angina we performed a quantitative angiographic evaluation of single, significant coronary stenoses (greater than 50%) during: spontaneous rhythm, graded atrial pacing (max 160 b/min) and at 1-3-5 min of recovery, both without drugs and after Ca-blockade (nifedipine, 10 mg sl). The greatest ST changes were at peak of the pacing in 9 patients (Group 1) and at recovery in 6 (Group 2). In each patient the stenotic lumen was reduced by atrial pacing (-9%, p less than 0.03); in Group 1 the lumen recovered soon after the end of the pacing, whereas in Group 2 narrowings became greater (-17%, p less than 0.02) at about 3 min of the recovery phase. In both groups nifedipine did not prevent the enhancement of the stenosis during pacing, but avoided constriction and ST changes during recovery in Group 2. Thus, in effort angina a superimposed active vasoconstriction contributes to the increase of the ST changes during the recovery phase of the exercise.

Aged↗
PubMed1990

[Acute coronary vasomotor effects of nifedipine and its therapeutic efficacy in syndrome X].

In 18 patients (12 females) presenting with effort-induced chest pain and normal coronary angiograms (syndrome X), 10 mg sublingual nifedipine increased the lumen of major coronary arteries (quantitative angiography) by 13% +/- 10 (p less than 0.01), coronary blood flow (thermodilution) by 23% +/- 26 (p less than 0.05), norepinephrine plasma concentration by 60% +/- 42 (p less than 0.01), and reduced the global ST segment shift during the effort stress test from 8.8 +/- 4.1 to 7 +/- 6.8 mm (p less than 0.03) at comparable maximal workload and at unchanged double product. There was a correlation (positive) of changes in flow with changes in coronary lumen diameter (r = 0.65, p less than 0.01), with ST segment response to exercise (r = 0.83, p less than 0.001), and with (inverse) norepinephrine plasma concentration (r = -0.70, p less than 0.01); no correlation was found between ST segment response and changes in arterial lumen diameter. In a few cases nifedipine did not improve or even worsened the response to exercise; in them coronary flow was unchanged or reduced and norepinephrine plasma levels were modestly or greatly increased, respectively. After 4-week treatment with nifedipine (10-20 mg 4 times daily), the effort ST segment shift was further diminished to 4.4 +/- 3.5 mm (p less than 0.03) despite a slightly increased double product. Plasma norepinephrine values, as compared to those following acute nifedipine, were reduced by 40% in patients with further improvement and unchanged in patients whose exercise performance did not vary.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[The flow-pressure relationship in coronary perfusion in myocardial hypertrophy in hypertension].

For any given perfusion pressure the difference between coronary autoregulated and maximally vasodilated flow represents the flow reserve. If hypertension and cardiac hypertrophy are present, the line of autoregulated flow becomes higher, and the pressure-flow relationship at maximal vasodilation less steep, due to the raised resistance. In these circumstances, flow reserve reduces and the point at which rest flow equals maximal achievable flow may be shifted to a higher perfusion pressure. Thus, flow would decline even if the perfusion pressure is lowered to normal. We tested this point in a setting of patients having chest pain and normal angiography of the left epicardial branches. Baseline flow (ml/min) from the great cardiac vein (thermodilution) was 142 +/- 13 in 9 normotensives (controls), 144 +/- 15 in 7 hypertensives (Group 1) with normal (114 +/- 11 g) left ventricular mass index and 188 +/- 17 in 8 hypertensives (Group 2) whose left ventricular mass (171 +/- 24 g) exceeded the mean +2 SD of normal. Coronary perfusion pressure was lowered in these patients by 5 mmHg every 5 minutes with a titrated nitroprusside infusion, taking as endpoints a perfusion pressure of 60 mmHg in the controls and of 70 mmHg in hypertensives. At endpoints, flow was similar to baseline in controls and Group 1. In Group 2 flow started to decline and myocardial oxygen extraction to slightly but significantly rise at perfusion pressure of from 90 to 80 mmHg; at the endpoint flow was reduced by 26% of baseline (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
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

Comparison of nifedipine, propranolol and isosorbide dinitrate on angiographic progression and regression of coronary arterial narrowings in angina pectoris.

Calcium antagonists and beta blockers may retard or inhibit atherogenesis. This study investigated whether nifedipine or propranolol influences coronary atherosclerosis in humans. In selected patients with effort angina and proven coronary artery disease, the cineangiographic pattern after 2-year therapy with nifedipine (group 1, 39 patients), propranolol (group 2, 36 patients) or isosorbide dinitrate (group 3, 38 patients) was compared to that before treatment. The disease evolved to a different extent in the 3 groups. Patients with evidence of progression of old narrowings and appearance of new narrowings were significantly fewer in group 1 (31% and 10%) than in group 2 (53% and 34%) and group 3 (47% and 29%). The number of stenoses with evidence of progression was significantly smaller after nifedipine (14), and larger after propranolol (39) compared with group 3 (24). Thus, nifedipine seemed more protective than the other 2 drugs against coronary atherosclerosis. The coronary risk factors were normal in the nifedipine group and remained so with treatment, suggesting that they were dissociated from influences on atherosclerosis. The evolution, as judged by the number of narrowings with progression, appeared significantly (p less than 0.01) worse with propranolol than with isosorbide dinitrate. Propranolol caused unfavorable modifications of serum lipids; there was a 28% increase in total triglycerides and a 25% decrease in high density lipoprotein cholesterol at 12 months in group 2.

Angina Pectoris↗
PubMed1989

Comparison of coronary vasomotor responses to nifedipine in syndrome X and in Prinzmetal's angina pectoris.

To test whether calcium channel blockade plays a similar role in the coronary vasomotion of patients with syndrome X (n = 29) and patients with Prinzmetal's angina pectoris (n = 12), quantitative angiography was used to evaluate the effect of nifedipine (10 mg, sublingually) on the lumen diameter of proximal, mid and distal thirds of normal epicardial branches. The main differences in the coronary vasomotor reaction were uniform vasodilatation in Prinzmetal's angina and a variable response to syndrome X, and a greater increase in the coronary lumen in patients with Prinzmetal's angina as compared with those with syndrome X who showed vasodilatation. The variable response in syndrome X was not related to changes in diastolic pressure and cardiac output. Patients showing coronary constriction were those who responded to nifedipine with a higher degree of tachycardia, which might suggest a neural participation in the paradoxic reaction to this drug. In the Prinzmetal group, on the contrary, at a similar heart rate increase the pattern was invariably vasodilatation. Thus, calcium ions appear to have a different role in the coronary smooth muscle contractility of the 2 series of patients; in fact, in Prinzmetal's angina nifedipine relaxed the coronary arteries to a greater degree and made them unresponsive to stimuli that were still able to cause vasoconstriction in patients with syndrome X.

Adult↗
PubMed1989

Effects of disopyramide on cycle length, effective refractory period and excitable gap of atrial flutter, and relation to arrhythmia termination by overdrive pacing.

The administration of class IA antiarrhythmic drugs facilities termination of atrial flutter by overdrive pacing. To investigate the electrophysiologic determinants of this effect, changes in the cycle length, the effective refractory period and the excitable gap of spontaneous type I atrial flutter were studied in 11 patients given intravenous disopyramide (3 mg/kg in 1 hour). After drug infusion, the cycle length of atrial flutter increased from 238 +/- 26 to 298 +/- 38 ms (+25%; p less than 0.001) and the effective refractory period prolonged from 169 +/- 19 to 192 +/- 25 ms (+14%; p less than 0.01). The excitable gap prolonged from 62 +/- 16 to 96 +/- 27 ms (+55%; p less than 0.001). Atrial flutter was terminated by overdrive pacing (mean cycle 203) in 10 of 11 patients; in 1 patient atrial fibrillation resulted after high rate stimulation. In the setting of an anatomically defined reentry circuit, as in type I atrial flutter, the administration of disopyramide prolongs both cycle length and refractory period. The finding of an increased excitable gap suggests that the drug exerts its prominent effect by depressing conduction velocity. A wider excitable gap allows easier penetration of the stimulus in the reentry circuit and accounts for the beneficial effects of type IA antiarrhythmic drugs on the termination of atrial flutter by overdrive pacing.

Aged↗
PubMed1989

Different coronary vasomotor effects of nifedipine and therapeutic correlates in angina with spontaneous and effort components versus Prinzmetal angina.

Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis has been considered a trigger for the spontaneous component of angina occurring both on effort and at rest. To investigate more thoroughly this pathophysiologic aspect we evaluated (by means of quantitative coronary angiography) the acute vasomotor reaction to nifedipine (10 mg sublingually) of significant (greater than 50%) stenotic lesions in 22 patients with double-component angina. We also correlated this reaction with the clinical response (daily number of ischemic episodes evaluated by means of 48-hour Holter ambulatory monitoring) to treatment with nifedipine (20 mg four times a day); calcium channel blockade, in fact, is considered a specific remedy in cases of altered coronary vasomotility. Patients with Prinzmetal angina, who were known to have homogeneous coronary vasodilating reactions and favorable clinical responses to nifedipine, were studied by means of the same methods and served as the control group (14 patients). In double-component angina the residual lumen diameter of significant lesions was unchanged in two patients, enhanced in 10, and reduced in 10 after sublingual nifedipine; lumen variations from baseline values ranged from +1.29 to -1.56 mm. Acute changes in stenosis correlated closely with results obtained with oral treatment. In the group with Prinzmetal angina, coronary stenoses invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of baseline); 100% of the patients in this group responded favorably to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Neural influences on the human pulmonary circulation as a defence reaction to volume depletion.

The role of the autonomic nervous system in the regulation of pulmonary vasomotility in man is unsettled and great emphasis is usually given to changes in flow as the main regulating mechanism. In order to simulate hypovolemia, which might reduce the mechanical influence of flow and disclose a neural mechanism, we decreased venous return through balloon distention in the inferior vena cava in 12 normal subjects, during right heart catheterization performed for diagnostic purposes. Caval obstruction was graduated to reduce cardiac output, right atrial and pulmonary arterial pressures, without altering systemic arterial pressure and heart rate. The sympathetic nervous system was activated by arithmetic and cold pressor tests. During the former, the increase in cardiac output was more than halved by venous return restraint, as compared to the unrestrained condition, and clear pulmonary vasoconstriction, instead of vasodilatation, was observed. During the cold test, cardiac output remained almost steady, in the absence as in the presence of balloon expansion. In both conditions pulmonary arteriolar resistance rose, but in the latter this increase was more than doubled. This study suggests that the autonomic nervous system is involved in the regulation of pulmonary vasomotility in man, its role being unveiled when the mechanical influence of flow is reduced by mimicking a hypovolemic state.

Adult↗
PubMed1989

Superior efficacy of propranolol versus nifedipine in double-component angina, as related to different influences on coronary vasomotility.

PURPOSE: In 24 patients with stable spontaneous and effort-related angina, ischemic episodes at rest were not preceded by changes in circulatory variables (heart rate, systemic and pulmonary arterial pressures) that may raise the myocardial oxygen consumption. We interpreted these episodes as caused by critical and reversible coronary flow reduction at the site of a stenotic lesion, and evaluated the clinical efficacy of nifedipine and propranolol in the treatment of this condition. PATIENTS AND METHODS: The study was randomized, placebo-controlled, and crossover in design. Nineteen of the 24 subjects were men (mean group age, 59 years; range, 47 to 65 years). The study consisted of four four-day periods. The first and the fourth periods, during which patients received placebo, were single-blind. The treatment consisted of 80 mg of propranolol or 20 mg of nifedipine administered four times daily. The second and the third periods, during which patients received propranolol or nifedipine crossing over to the alternative drug in the next period, were double-blind and separated by a 24-hour interval. RESULTS: Propranolol fully abolished or reduced the number of spontaneous ischemic episodes in a significantly larger proportion of patients than did nifedipine; it was also effective in several cases in which nifedipine had failed or had even caused a paradoxic effect. Quantitative angiographic evaluation of the influences of nifedipine (Group 1, 12 patients, 10 mg sublingually) and propranolol (Group 2, 12 patients, 0.1 mg/kg intravenously) on the residual lumen diameter of one significant coronary stenosis in each patient showed that (1) after nifedipine, the lumen was unchanged in one, augmented in seven, and reduced in four cases; (2) variations ranged between +1.59 and -1.2 mm, and their direction correlated closely with the influence of oral nifedipine on the episodes of spontaneous ischemia; and (3) in no case did treatment with propranolol vary the stenosis lumen by more than 0.3 mm. CONCLUSION: In this form of angina, a number of lesions seem to offer a compliant substrate for vasomotion and, possibly, for critical changes in flow. The vasomotor influences of nifedipine on these lesions are variable as well as the efficacy of the drug on the manifestations of ischemia at rest. Propranolol produces no important variations of the coronary stenotic lesions, causes a decrease of heart rate that facilitates coronary flow in diastole, and reduces the baseline metabolic demand of the heart so that the threshold of ischemia during critical reduction of coronary flow may become elevated.

Aged↗
PubMed1989

Neural influences on the pulmonary vascular bed in man.

1. Impedance to venous return by distention of a balloon in the inferior vena cava (IVCB) was utilized in 10 patients, during diagnostic procedures, to reduce blood flow through the lungs at baseline and to buffer its changes during stimulation of the adrenergic system, which was obtained with mental arithmetic (AT) and cold pressor (CPT) tests. 2. When venous return was unimpeded, cardiac output rose by 2.06 1/min during the AT and remained steady during the CPT, and arteriolar resistance in the pulmonary circuit was significantly reduced and slightly raised, respectively. 3. During IVCB, baseline cardiac output decreased by 710 ml/min, it rose by 925 ml/min during the AT and again remained steady during the CPT; pulmonary arteriolar resistance was unchanged from before obstruction at baseline and was significantly augmented by both tests. In particular, AT became a clear vasoconstrictor stimulus, having originally produced vasodilatation. 4. These observations support the view that lung blood vessels in man are sensitive to adrenergic influences and that vasoconstriction can be elicited in circumstances in which the flow through the lungs is restrained. The physiological importance of the neural regulation of the pulmonary circulation in man remains undefined.

Adult↗
PubMed1989

Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure.

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.

Adult↗