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Biomedical subjects

A P Niarchos

Publications and source records attributed to A P Niarchos.

At least 19 recordsLinked to original sources
PubMed2000

Resolution of ST-segment elevation after streptokinase therapy in anterior versus inferior wall myocardial infarction.

BACKGROUND: Resolution of ST-segment elevation is the best bedside predictor of myocardial reperfusion. HYPOTHESIS: This study was conducted to examine the resolution of ST-segment elevation after streptokinase therapy in anterior versus inferior acute myocardial infarction (MI) and to corroborate it with echocardiographic and coronary angiographic data. METHODS: The study population consisted of 70 patients, 35 each in the anterior and inferior MI groups. The electrocardiograms (ECGs) were recorded before, on completion of, and on Days 1 and 2 post streptokinase therapy. The resolution of ST segment determined from post-streptokinase ECGs was compared between the two groups and correlated with echocardiographic and coronary angiographic data. RESULTS: On completion of and on Day 1 post streptokinase therapy, ST-segment resolution in both groups was not significantly different. On Day 2 post streptokinase therapy, resolution of the ST segment per lead was significantly lower in anterior than that in inferior MI (61 +/- 21% anterior vs. 77 +/- 21% inferior, p 0.003). The number of patients with akinesis of infarct-related ventricular wall was significantly higher (17 anterior vs. 7 inferior, p 0.02), and left ventricular ejection fraction was significantly lower in anterior MI (39 +/- 7% anterior vs. 48 +/- 8% inferior, p < 0.01). There was no significant difference in coronary angiographic data. One patient in each group demonstrated normal coronary arteries. CONCLUSIONS: The resolution of ST-segment elevation on the completion of and on Day 1 post streptokinase therapy was comparable between anterior and inferior MI. The significantly less frequent resolution of ST-segment elevation in anterior MI on Day 2 post streptokinase could be due to more akinesis, larger infarct size, and worse systolic function rather than due to failure to open the infarct-related vessel.

Coronary Angiography↗
PubMed1985

Angiotensin I converting enzyme activity in hypertension. Relationship to blood pressure, renin-sodium profiles, and antihypertensive therapy.

The activity of the angiotensin I converting enzyme was measured in 55 patients with untreated essential hypertension, 11 patients with untreated renovascular hypertension, five patients with untreated primary aldosteronism, and 23 normotensive subjects. Converting enzyme activity was significantly higher (p less than 0.025 or less) in essential hypertension (28 +/- 1 units/ml) and renovascular hypertension (28.5 +/- 3 units/ml) when compared with the activity in the normotensive subjects (21 +/- 1.5 units/ml). Seventeen (31 percent) of the patients with essential hypertension and three (27 percent) patients with renovascular hypertension had an elevated converting enzyme activity above the mean +2 standard deviations value of the normotensive subjects (32.8 units/ml), ranging from 33 to 55.8 units/ml. Converting enzyme activity was similar in black and white patients and in male and female patients, but it tended to decrease with increasing age in both the hypertensive and the normotensive subjects. In the untreated patients with essential hypertension (n = 55), converting enzyme activity was inversely related to mean arterial pressure and age (r = -0.34, p less than 0.01) and positively related to plasma renin activity (r = 0.31, p less than 0.05). Converting enzyme activity was always decreased during captopril therapy, and it was not affected by beta blockers, but it was increased by diuretics. These findings indicate that converting enzyme activity is elevated in patients with essential and renovascular hypertension.

Adolescent↗
PubMed1984

Hemodynamic effects of nifedipine versus hydralazine in primary pulmonary hypertension.

The acute hemodynamic effects of both sublingual nifedipine (N) and intravenous hydralazine (Hy) were studied in 5 patients with primary pulmonary hypertension to ascertain whether the capacity for pulmonary vasodilatation was generalized or drug-specific, and to determine which of the 2 agents had preferential pulmonary vasodilatory effects. For the group as a whole, neither N nor Hy produced changes in heart rate, mean pulmonary capillary wedge or right atrial pressures. Both N and Hy reduced mean systemic arterial pressure (before N 90 +/- 8 mm Hg, after N 76 +/- 7 mm Hg, p less than 0.01; before Hy 92 +/- 11 mm Hg, after Hy 68 +/- 8 mm Hg, p less than 0.05), and decreased systemic vascular resistance (before N 1,558 +/- 645 dynes s cm-5, after N 1,192 +/- 430 dynes s cm-5, p less than 0.05; before Hy 1,700 +/- 415 dynes s cm-5, after Hy 957 +/- 285 dynes s cm-5, p less than 0.05). In addition, N administration resulted in an increased cardiac output (before N 4.5 +/- 2.0 liters/min, after N 4.8 +/- 2.0 liters/min, p less than 0.01); Hy administration was associated with a more varied effect on cardiac output (before Hy 4.0 +/- 1.0 liters/min, after Hy 5.3 +/- 1.8 liters/min, p less than 0.10, difference not significant [NS]).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1984

Effects of diuretic therapy in low-, normal- and high-renin isolated systolic systemic hypertension.

In 30 patients with isolated systolic systemic hypertension, diuretic therapy decreased body weight from 71.33 +/- 2.67 to 70.37 +/- 2.65 kg (p less than 0.0005) and the systolic blood pressure from 174 +/- 3 to 156 +/- 3 mm Hg (p less than 0.0005). Diastolic blood pressure and heart rate did not change significantly. Plasma renin activity increased from 2.25 +/- 0.33 to 4.27 +/- 0.43 ng/ml/hour (p less than 0.0005) and urinary aldosterone from 9 +/- 1 to 16 +/- 2 micrograms/24 hours (p less than 0.005). The antihypertensive effect of diuretics was significantly related only to the pretreatment plasma renin activity (r = -0.50, n = 30, p less than 0.05), and therefore the greatest decrease in systolic blood pressure occurred in the low-renin group, whereas the smallest occurred in the high-renin group (-22 +/- 2 vs -3 +/- 9 mm Hg, p less than 0.005). The diastolic blood pressure was significantly decreased only in the low-renin group (-7 +/- 2 mm Hg, p less than 0.005). There were no significant changes in blood pressure in 11 untreated control patients. These results indicate that diuretics are effective antihypertensive agents in most patients with low- and normal-renin isolated systolic systemic hypertension.

Adult↗
PubMed1984

Renin dependency of blood pressure in isolated systolic hypertension.

The role of the renin system in the maintenance of the elevated systolic blood pressure in isolated systolic hypertension was investigated in 31 patients who received long-term treatment with propranolol (120 mg daily) and in another group of 22 patients with isolated systolic hypertension who received a test dose of captopril (25 or 50 mg). The greatest systolic blood pressure decrease (35 +/- 5 mm Hg) by propranolol occurred in the high-renin group (n = 9), and the smallest decrease (3 +/- 2 mm Hg) in the low-renin group (n = 9), whereas in the normal-renin group (n = 13), systolic blood pressure was decreased by propranolol by 22 +/- 5 mm Hg. For all the propranolol-treated patients, the decrement in the systolic blood pressure by propranolol was related to the control plasma renin activity (r = 0.63, p less than 0.01) and to the concurrent change in plasma renin activity (r = 0.70, p less than 0.001). Captopril decreased the systolic blood pressure by 55 +/- 10 mm Hg in the high-renin group (n = 11) and by 17 +/- 5 mm Hg in the normal-renin group (n = 6), whereas the smallest decrease (12 +/- 5 mm Hg) in systolic blood pressure occurred in the low-renin group (n = 5). In all the captopril-tested patients (n = 22), the decrease in systolic blood pressure by captopril was related to the control plasma renin activity (r = 0.75, p less than 0.001). These results indicate that the plasma renin activity value indicates the participation of the renin-angiotensin system in the maintenance of the elevated systolic blood pressure in patients with isolated systolic hypertension.

Adult↗
PubMed1984

Comparison of the effects of diuretic therapy and low sodium intake in isolated systolic hypertension.

Of 103 patients with isolated systolic hypertension, 71 were treated with diuretics and another 32 with low-sodium diet. In the 71 who were treated with diuretics, body weight decreased from 69.48 +/- 1.47 to 68.60 +/- 1.45 kg (p less than 0.0005) and systolic blood pressure from 178 +/- to 152 +/- 2 mm Hg (p less than 0.0005). Plasma renin activity increased from 1.78 +/- 0.30 to 7.32 +/- 1.78 ng/ml per hour (p less than 0.005) and urinary aldosterone from 10 +/- 1 to 23 +/- 4 micrograms per 24 hours (p less than 0.005). The greatest decrease in systolic blood pressure occurred in patients in the low-renin group (-32 +/- 2 mm Hg), whereas it decreased by 24 +/- 2 mm Hg (p less than 0.04) in the normal-renin group; however, blood pressure did not change significantly in the high-renin group. In the 32 patients who were treated with low-sodium diet, the 24-hour urinary sodium excretion decreased from 143 +/- 10 to 48 +/- 5 meq (p less than 0.005), body weight decreased from 71.18 +/- 2.50 to 70.17 +/- 2.47 kg (p less than 0.005), systolic blood pressure decreased from 174 +/- 2 to 156 +/- 3 mm Hg (p less than 0.0005), and diastolic blood pressure decreased from 90 +/- 1 to 87 +/- 1 mm Hg (p less than 0.01). Plasma renin activity increased from 2.25 +/- 0.33 to 4.27 +/- 0.43 ng/ml per hour (p less than 0.005) and urinary aldosterone from 9 +/- 1 to 15 +/- 2 micrograms per 24 hours (p less than 0.005). The decrease in the systolic blood pressure was related to the pretreatment 24-hour urinary sodium excretion (r = 0.40, p less than 0.05). The smallest decrease in systolic blood pressure occurred in the patients with high renin values (-1 +/- 9 mm Hg, n = 5), whereas the decrease in systolic blood pressure in the low-renin (n = 12) and normal-renin groups (n = 15) was similar, -22 +/- 2 mm Hg and -21 +/- 3 mm Hg, respectively (p less than 0.005 compared with the high-renin group). These results indicate that both diuretic therapy and low-sodium diet are effective antihypertensive means in most patients with isolated systolic hypertension and low or normal plasma renin activity.

Adult↗
PubMed1983

Hemodynamic effects of massive peripheral edema.

The possibility that noncardiac massive peripheral edema reduces venous distensibility was investigated in eight patients in the supine and 80-degree head-up tilt position before and after diuretic therapy. After clearance of the edema with diuretic therapy, total blood volume (TBV) was not significantly decreased; therefore, in the supine position the significant (2p less than 0.001) decrease of right atrial pressure, stroke volume, cardiac output, and cardiopulmonary blood volume (CBV) by the diuretics was due to an improvement in venous compliance which resulted in peripheral redistribution of CBV since the ratio CBV/TBV was decreased during diuretic therapy (2p less than 0.001). Furthermore, before diuretic therapy, tilt significantly decreased right atrial pressure, stroke volume, cardiac output, CBV, and the ratio CBV/TBV; but after diuretic therapy, the decrease of the same variables during tilt was significantly (2p less than 0.001) greater. These results indicate that marked peripheral edema considerably decreases venous compliance which can be improved with diuretic therapy.

Adult↗
PubMed1982

Hemodynamic effects of captopril in pulmonary hypertension of collagen vascular disease.

Captopril 12.5 to 50 mg as a single dose was given to six patients with pulmonary hypertension secondary to collagen vascular disease. Total pulmonary resistance was decreased in four patients from 19% to 39%, but mean pulmonary artery pressure (63 +/- 15 mm Hg) was not decreased, probably because of the concurrent increase in cardiac output from 21% to 52% (2p less than 0.05). The systemic arterial pressure was slightly decreased due to the decrease in total systemic resistance. Control plasma renin activity ranged from 0.15 to 16 ng/ml/hr and was increased during captopril from 19% to 356%. These results, although preliminary, suggest that captopril may be beneficial in certain patients with pulmonary hypertension secondary to collagen vascular disease.

Adult↗
PubMed1982

Hemodynamic effects of diuretics in patients with marked peripheral edema and mild hypertension.

Hypertension develops in about 10% to 50% of patients with nephrosis or cirrhosis and peripheral edema, but the hemodynamic mechanism of the hypertension and its reversal by diuretic therapy has not been elucidated. In eight patients with marked edema and mild hypertension, diuretics (furosemide and spironolactone) decreased mean arterial pressure because of concurrent decrease in cardiac output and total peripheral resistance. Neither total blood volume nor plasma volume were decreased by the diuretics and the decrease in body weight was therefore attributed to the decrease in interstitial fluid volume. This, in turn, resulted in increased venous capacitance (as can be judged from the diuretic-induced decrease in the ratio of cardiopulmonary blood volume/total blood volume).

Adult↗
PubMed1982

Plasma catecholamines and cardiovascular responses during converting enzyme inhibition in normotensive and hypertensive man.

The hemodynamic and plasma catecholamine responses to isometric exercise and head up tilt were investigated in normotensive and hypertensive subjects during normal and low sodium intake and before and during the administration of the converting enzyme inhibitors teprotide or captopril. Although teprotide and captopril decreased significantly the mean arterial pressure during both sodium intakes the normal pattern of hemodynamic response to hand grip and head up tilt was preserved. Moreover changes of plasma catecholamines during hand grip and head up tilt were not affected either by teprotide or captopril. When following the administration of teprotide or captopril fainting occurred either in the seated position or during head up tilt it was associated not only with a decrease in arterial pressure but also with a concurrent reduction in cardiac output and/or hypovolemia. It is concluded that converting enzyme inhibition does not impair significantly the cardiovascular responses which are mediated via the sympathetic nervous system either in normotensive or in hypertensive subjects.

Adult↗
PubMed1982

The vasoconstriction-volume spectrum in normotension and in the pathogenesis of hypertension.

A body of evidence has been reviewed indicating that all hypertensive phenomena ranging from mild disorders to fulminant malignant hypertension can be profitably analyzed by assessing the relative contribution of two final determinants of the arterial blood pressure--the vasoconstriction and volume components. Renin-sodium profiling and the separate application of specific pharmacologic probes provide the basic tools for identifying the relative contribution of the two components. For an equal degree of hypertension, volume forms appear to exhibit better organ flow than the more vasoconstricted forms. This bidimensional analysis has provided new understanding of the pathophysiological mechanisms of the spectrum of human hypertensive diseases of practical value for the evaluation, diagnosis, and treatment of individual patients. Beyond this, the analytical scaffold identifies some key questions for future research.

Aldosterone↗
PubMed1980

Hemodynamic effects of the converting enzyme inhibitor teprotide in normal- and high-renin hypertension.

The hemodynamic effects of the converting enzyme inhibitor teprotide (SQ 20881) were investigated in five patients with normal plasma renin activity who were normotensive during the study (group I), in five patients with hypertension and normal plasma renin activity (group II), and in five patients with hypertension and high plasma renin activity (group III). No significant hemodynamic changes were observed during teprotide administration in group I. In group II there was a decrease in mean arterial pressure by 10 +/- 2% (p < 0.005) that was associated with a decrease by 16 +/- 7% (p < 0.05) in stroke volume and cardiac output, possibly due to venodilatation and without a concurrent change in total peripheral resistance. In group III the larger decrease of 19 +/- 4% (p < 0.005) in mean arterial pressure was due to a decrease by 30 +/- 3% (p < 0.005) in peripheral resistance. In this group stroke volume and cardiac output increased by 13 +/- 2% (p < 0.025). There were no compensatory changes in heart rate despite the decrease in mean arterial pressure and vasodilatation. These results indicate that teprotide decreases arterial pressure by a dual hemodynamic mechanism. Cardiac output is increased by teprotide in patients with high-renin hypertension who exhibit the greatest decrements in peripheral resistance.

Adult↗