Biomedical subjects

F Fabbiocchi

Publications and source records attributed to F Fabbiocchi.

At least 37 records · Page 2Linked to original sources

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↗

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↗

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

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

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

Electrophysiologic and haemodynamic correlates in supraventricular tachycardia.

In 16 subjects with paroxysmal supraventricular tachycardia (SVT) we sought a relationship between haemodynamic changes associated with artificially induced arrhythmias and the electrophysiological properties of the related atrioventricular (AV) nodal reentry circuit. In 10 patients (group 1) induced SVT was typical (long AH) and caused a significant fall in cardiac output (-1.720 ml min-1) and arterial systolic pressure (-18 mmHg). In six subjects (group 2), induced SVT was atypical (long HA) and did not significantly alter the output of the heart and systolic pressure, despite the elicitation of similar tachycardia. The opposite AV nodal reciprocation pattern which resulted in a substantial increase in AH/HH in group 1 and in a slight rise of the same variable in group 2, may explain these haemodynamic differences. In fact, atrial and ventricular systoles occurred simultaneously and impeded the ventricular filling in the former group, while a regular subsequence of contraction was maintained in the latter group. In group 2, systolic arterial pressure and cardiac output fell to the same level as in group 1 when right atrial pacing, at a similar rate of SVT, determined an increase of AH/HH similar to that observed during typical tachycardia. Thus, the haemodynamic response to SVT differs significantly between the two types of reciprocating tachycardia, particularly as regards cardiac output and blood pressure, and is mainly influenced by the temporal relationship between atrial and ventricular systole, independent of the rate of contraction. The different conduction velocities of the reciprocating circuit limbs and their interrelation seem to be major determinants of the haemodynamic pattern of SVT.

Adult↗

PubMed1989

Different vasomotor action of nifedipine on dynamic coronary obstructions and therapeutic response in effort and prinzmetal angina.

Variations induced by nifedipine (10 mg sublingually) in the residual lumen diameter of significant (greater than 50%) coronary lesions were assessed angiographically in 58 patients with effort angina (group 1) and in 19 patients with Prinzmetal angina (group 2). A relationship was sought between these acute variations of the stenotic lumen and the clinical response to treatment with the same drug (20 mg four times daily). Treatment efficacy was evaluated with exercise testing in group 1 and Holter monitoring in group 2. In group 1 the residual segment of stenotic diameter showed an increase, decrease, or no change with the calcium antagonist. Nifedipine failed to improve 40% of the cases (21% unchanged and 19% worsened) in group 1. In the same group of patients, the responses to exercise tests were dissociated from the acute vasomotor pattern. Changes in the pressure-rate product also did not explain the clinical results. In group 2 the majority of lesions had compliant portions, which invariably reacted to nifedipine with dilatation. All patients with the Prinzmetal form had relief of the anginal episodes with treatment. These data suggest that the therapeutic efficacy of nifedipine in classic effort angina probably is the net result of influences on the myocardial oxygen consumption and supply, and the acute coronary vasomotor pattern does not allow to predict the clinical response. Stenotic lesions in the Prinzmetal form possess a distinct sensitivity to the relaxant action of calcium channel blockade, which reasonably explains the highly positive response to treatment.

Adult↗

PubMed1989

[Activation and inhibition of adrenergic effects on the coronary vessels of patients with different forms of angina pectoris].

Experimental data in animals indicate that coronary vasoconstriction occurs following blockade of the beta-adrenergic receptors or alpha-receptors activation. The vasomotor effects of these maneuvers in man are unclear. Therefore we investigated whether and to which extent alpha-stimulation (cold pressor test: CPT) and beta-blockade (propranolol) cause coronary vasoconstriction; whether this effect involves the resistance arterioles as well as the large epicardial branches, and, within these, whether the normal and stenotic tracts are involved. Patterns in patients with effort angina were compared with those in patients with Prinzmetal angina. We studied 19 cases with classic and 15 cases with Prinzmetal angina. The systemic, pulmonary and coronary hemodynamics (pressure, flow and resistance) and the vasomotor pattern of normal and stenotic epicardial branches (quantitative angiography) were evaluated in the baseline condition, during CPT, after propranolol (5 mg iv) and during CPT repeated after propranolol. We observed that: changes of the coronary flow due to beta-blockade and to CPT are related to the variations of the myocardial oxygen consumption, induced by the inhibition and activation of adrenergic receptors and not to the concomitant vasomotor reaction of the stenotic vascular tract; beta-blockade does not affect homogeneously the lumen of the stenotic lesions in effort angina and invariably increases the lumen in the Prinzmetal form; influences of CPT, in the absence as well as in the presence of beta-receptor blockade, on the lumen diameter of both normal vessels and stenotic lesions are minimal in either form of angina.

Angina Pectoris↗

PubMed1989

[Greater efficacy of propranolol versus nifedipine in angina with 2 components, that results in varying influence on coronary vasomotility].

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 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. Propranolol fully abolished or reduced the number of spontaneous ischemic episodes in a significantly larger number of patients than did nifedipine; it was also effective in several cases in whom nifedipine had failed or had even caused a paradoxic effect. Quantitative angiographic evaluation of the influence 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 1 significant coronary stenosis in each patient showed that after nifedipine, the lumen was unchanged in 1, augmented in 7, and reduced in 4 cases; 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 in no case did treatment with propranolol vary the stenosis lumen by more than 0.3mm. 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.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina Pectoris↗

PubMed1989

[Various clinical and vasomotor coronary responses to calcium block in mixed angina and Prinzmetal's angina, expression of various physiopathologic mechanisms].

Impedance to flow due to coronary spasm is currently interpreted as the mechanism of Prinzmetal angina. Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis is also viewed as the trigger for the spontaneous component of mixed angina. The major question that we attempted to answer in this study was whether mixed angina may be considered a variant of the Prinzmetal form, or a particular manifestation of the classic effort form. For these purposes we investigated the acute vasomotor response to calcium channel blockade (nifedipine 10 mg sl) of both significant (greater than 50%) stenotic lesions and of normal coronary vessels in 22 patients with mixed angina and in 14 patients with Prinzmetal angina, and correlated it with the clinical response to treatment (nifedipine 20 mg qid). Calcium channel blockade, in fact, is considered as a specific remedy in the presence of an altered coronary vasomotility. The clinical response was evaluated through ambulatory Holter monitorings of 48 hour duration, while on placebo, nifedipine and placebo again. In mixed angina an angiographic evaluation showed that the residual lumen diameter of significant lesions was unchanged in 2, enhanced in 11 and reduced in 9 patients after sl nifedipine; lumen variations from base line ranged from +1.5 to -1.3 mm. Acute stenosis widening or narrowing correlated closely with the efficacy or not of the treatment. In the Prinzmetal group the vast majority of the lesions had compliant portions which invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of base line); 100% of patients in this group responded favourably to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

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↗

PubMed1989

[Comparison of the coronary vasomotor response to nifedipine in syndrome X and in Prinzmetal's angina].

In this study we tested whether Ca++ has a similar part in the coronary vasomotion of patients with syndrome X (n = 29) and patients with Prinzmetal angina pectoris (n = 12). Through quantitative angiography we evaluated the influence of nifedipine (10 mg sl) 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 angina and a variable response in syndrome X; greater increase in the coronary lumen in patients in the former as compared to those in the latter group 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; this might suggest a neural participation in the paradoxical reaction to this drug. In the Prinzmetal group, on the contrary, at 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 angina nifedipine relaxed the coronary arteries more potently and made them unresponsive to stimuli which were still able to cause vasoconstriction in syndrome X.

Adult↗

PubMed1988

Coronary vasomotor and clinical effects of nifedipine in effort, mixed and Prinzmental angina.

Changes induced by nifedipine (10 mg s.l.) in the residual lumen diameter of significant (greater than 50%) coronary lesions were assessed angiographically in 69 patients with effort angina (Group 1), in 22 patients with mixed angina (Group 2), and in 14 patients with Prinzmental angina (Group 3). These changes were related to the clinical response to treatment with the same drug (diary records, exercise testing, Holter monitoring). In Groups 1 and 2 segments of stenotic vessels showed either increase, decrease or no change in diameter with the calcium antagonist; in Group 3 the majority of the vessels showed compliant portions which invariably responded with dilatation. Nifedipine failed to improve cases with exertional (21% unchanged, 19% worsened) and mixed (41% exacerbated) forms; all patients with the Prinzmental form had relief of the anginal episodes. In Group 1, the response to exercise tests were dissociated from the acute vasomotor pattern and the pressure-rate product failed to explain the clinical results. Fifty-two percent of the patients in Group 2 showed significant acute widening of critical stenoses as well as obvious improvement; patients in this group who did worse with treatment had reacted to nifedipine with narrowing of their critical stenoses. These data suggest that: the response to nifedipine of classic effort angina is probably the net result of an interaction of changes in myocardial oxygen consumption and supply; coronary vasomotion has a role in mixed angina and influences of nifedipine may be either favorable or unfavorable; stenotic lesions in the Prinzmental form are quite sensitive to the relaxant action of calcium blockade and this probably represents a background to the highly positive clinical response to treatment.

Angina Pectoris↗