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  • 1
    ISSN: 1432-1440
    Keywords: Isosorbide dinitrate ; Angina pectoris ; Sustained therapy ; Nitrate tolerance ; Exercise testing
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Ten patients with angiographically proven coronary heart disease, stable exercise-induced angina pectoris, and reproducible ST-segment depression were treated with isosorbide dinitrate (ISDN) tablets in daily doses of 240 mg (6×40 mg) and placebo (PL) for 28 days each on the basis of a randomized double-blind protocol with intraindividual cross-over. ISDN treatment resulted in a sustained reduction of anginal attacks with a weekly mean rate ranging from 1.4 (3rd week) to 3.9 (4th week) as compared to 10.2 (2nd week) to 11.7 (4th week) during placebo treatment (P〈0.001). Ischemic response during stress testing (sum of ST-segment depressions) was significantly improved during ISDN treatment as compared to placebo. Day 1: 56% (P〈0.01); day 7: 30% (P〈0.01); day 28: 49% (P〈0.001). Heart rate and arterial blood pressure in the upright position were different between ISDN and placebo on day 1 and day 7 of the treatment phases (P〈0.02), but not on day 28. Nitrate responsiveness with regard to blood pressure and heart rate was restored after a drug-free interval of 2 days. The plasma concentrations for ISDN and the mononitrate metabolites exhibited a constant ratio during the treatment period. Thus, therapy with 6 × 40 mg ISDN per day resulted in a sustained reduction of anginal attacks and preserved improvement of ischemic ST-segment depression during exercise in upright position.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 65 (1987), S. 69-75 
    ISSN: 1432-1440
    Keywords: Hyperkinetic heart syndrome ; Bradycardic drugs ; Alinidine (ST 567) ; Propranolol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A hyperkinetic heart syndrome has been diagnosed in 10 patients by clinical investigation and right-heart catheterization at rest and during exercise. Subsequently, the patients received 3×40 mg alinidine, and 2×40 mg propranolol and placebo, each for 2 weeks in a double-blind cross-over study. Heart rate at rest (P〈0.05) and during exercise (P〈0.001) decreased significantly under alinidine and propranolol to the same extent (control, 83/170; alinidine, 68/146; propranolol, 73/139; placebo, 83/162 beats per min). Lower limb flow at rest and after exercise, measured by plethysmography, as well as left-ventricular fractional shortening and mean velocity of circumferential fiber shortening, measured by echocardiography, decreased insignificantly. Sedation and a dry mouth occurred in six patients under alinidine, while fatigue and cold hands and/or feet were reported by five patients under propranolol. Thus, alinidine may be used as an alternative to beta-blocking in the treatment of the hyperkinetic heart syndrome.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 77-85 
    ISSN: 1432-1440
    Keywords: Molsidomine ; Acute myocardial infarction ; Left- and right ventricular filling pressure ; ST-segment elevation ; Molsidomin ; Frischer Herzinfarkt ; Links- und rechts-ventrikulärer Füllungsdruck ; ST-Hebung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die hämodynamische Wirkung von Molsidomin und der Effekt auf die Myokardischämie wurde bei 48 Patienten mit frischem Herzinfarkt untersucht. In einer Dosierung von 8–12 mg in oraler und intravenöser Form führte Molsidomin zu einer signifikanten Senkung des linksventrikulären Füllungsdruckes. Bei Patienten mit einem Füllungsdruck unter 20 mm Hg fiel der diastolische Pulmonalarteriendruck bei 2×4 mg oral von 12,1 auf 8,8 mm Hg. Bei Patienten mit Linksinsuffizienz und linksventrikulärem Füllungsdruck über 20 mm Hg (Gruppe 2) wurde nach 12 mg intravenös eine Senkung des Füllungsdruckes von 23,8 auf 17,4 mm Hg erreicht. Es kam außerdem zu einer signifikanten Reduktion des rechten Vorhofdruckes in allen Dosisbereichen. Während bei nicht linksinsuffizienten Patienten (Gruppe 1) eine Reduktion des Herzminutenvolumens beobachtet wurde (5,7 auf 4,7 l/min) blieb das Herzminutenvolumen in Gruppe 2 unverändert. Die Herzfrequenz nahm in Gruppe 2 von 85 auf 81/min ab. Der arterielle Blutdruck reduzierte sich nur unter der höheren Dosierung um 10 mm Hg im Mittel, während in niedriger Dosierung der Blutdruck unverändert blieb. Der periphere Widerstand änderte sich dabei nicht. Die Vollwirkung war 30 min nach oraler Applikation erreicht. Drei Stunden später war die Wirkung auf die Hälfte reduziert. Nach 8 h war der Effekt nur noch minimal. Die Nebenwirkungsrate war gering, kurzfristige Kopfschmerzen traten nur bei 8% der Patienten auf. Beim intraindividuellen Vergleich mit 1,6 mg Nitroglycerin sublingual fand sich kein signifikanter Unterschied in der hämodynamischen Wirksamkeit (n=11). Molsidomin hat ähnlich wie Nitroglycerin einen günstigen Effekt auf die Hämodynamik und Myokardischämie. Es kommt primär zur Verminderung der Vorlast. Auch der mäßige Effekt auf die Nachbelastung mit geringer Senkung des arteriellen Druckes bei höheren Dosierungen kann als vorteilhaft angesehen werden.
    Notes: Summary The effect of molsidomine on hemodynamics and myocardial ischemia were studied in 48 patients with acute myocardial infarction. Between 8 and 12 mg of orally and intravenously administered molsidomine led to a significant reduction in left ventricular filling pressure. In response to 2×4 mg p.o., diastolic pulmonary arterial pressure fell from 12.1 to 8.8 mm Hg in patients with filling pressure below 20 mm Hg. Patients with left heart failure and left ventricular filling pressure above 20 mm Hg (Group 2) displayed a decline in filling pressure from 23.8 to 17.4 mm Hg following 12 mg i.v. In addition, right atrial pressure dropped significantly across the entire range of dosages. Although patients without left ventricular failure (Group 1) showed a decline in cardiac output (5.7 to 4.7 l/min), this parameter remained unchanged in Group 2. Heart rate in Group 2 fell from 85 to 81 per min. Arterial blood pressure was reduced by a mean of only 10 mm Hg at high dosages and remained unchanged at lower dosages. No change was observed in peripheral resistance. The maximum effect was seen 30 min after oral administration. Three hours later, the effect was reduced by half. Only minimal activity could be observed after 8 h. The incidence of side effects was low, with transient headaches occurring in 8% of the patients. An intraindividual comparison with 1.6 mg of sublingually administered nitroglycerin demonstrated no significant difference in hemodynamic effectiveness (n=11). Molsidomine, not unlike nitroglycerin, exerts a favorable effect on hemodynamics and myocardial ischemia. It acts primarily to reduce preload. The additional moderate effect on afterload with a slight decline in arterial pressure at high dosages may also be considered advantageous.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 1. Measurements of blood flow in the calf muscle of healthy men are reported. 2. Muscle clearance of Xenon 133, plethysmography and electronic oscillography were used as methods. 3. The blood flow was measured at rest in the supine position, after 3 min ischemia, during and after maximal muscle exercise and after exercise combined with ischemia. The muscle exercise was always performed until the person noted muscle pain. 4. After 3 min of ischemia the muscle blood flow was 4–8 times higher than at rest, 16–22 times higher during and after exercise, and after exercise combined with ischemia 17–25 times higher than at rest. Statistically there was only a difference between ischemia and exercise but not between exercise and exercise combined with ischemia. 5. The duration of elevated blood flow was less than 2 min after ischemia and more than 10 min after maximal exercise with or without ischemia. 6. The obtained values of muscle blood flow at rest, during and after exercise were within the limits obtained by other authors. Muscle blood flow estimated by the Xenon 133 clearance method gave consistently higher results than by plethysmography. The increase in blood flow in relation to the flow at rest however was the same with both methods. 7. The results show that for clinical evaluation of muscle blood flow in the human calf, flow measurements at rest are inaccurate because the rest flow is only about 1/20 of the maximal flow. 8. A maximal muscle blood flow in healthy subjects can be produced by exercise, but not by ischemia alone; after maximal exercise combined with ischemia the flow is not essentially higher than after maximal exercise without ischemia.
    Notes: Zusammenfassung 1. Es wird über Durchblutungsmessungen am Unterschenkel gesunder Personen berichtet. 2. Methodisch wurde neben der Verstärker-Oscillographie die Venenverschluß-Plethysmographie und die Gewebsclearance von Xenon133 benützt. 3. Es wurde die Ruhedurchblutung und die Durchblutung nach arterieller Drosselung, nach Muskelarbeit und nach ischämischer Muskelarbeit gemessen. Die Muskelarbeit erfolgt jeweils bis zum Auftreten von Schmerzen. 4. Die erreichte Mehrdurchblutung betrug nach arterieller Drosselung das Vier- bis Achtfache des Ruhewertes, nach Muskelarbeit das Sechzehn- bis Zweiundzwanzigfache und nach ischämischer Arbeit das Siebzehn- bis Fünfundzwanzigfache des Ruhewertes. Statistisch war nur die Differenz zwischen arterieller Drosselung und Muskelarbeit zu sichern. 5. Die Dauer der reaktiven Hyperämie war nach Drosselung sehr kurz. Nach 1/4 min konnte die Mehrdurchblutung schon nicht mehr voll erfaßt werden, nach 2 min war sie weitgehend abgeklungen. Nach Muskelarbeit hielt die reaktive Hyperämie dagegen länger als 10 min an. 6. Die gefundenen Absolutwerte der Durchblutung in Ruhe und nach Belastung werden mitgeteilt, sie decken sich mit den Literaturangaben. 7. Für die Klinik wird gefolgert, daß eine Messung der Ruhedurchblutung unzureichend ist, da sie nur etwa ein Zwanzigstel der möglichen Durchblutung beträgt. 8. Die Durchblutungsreserve ist — zumindest bei Gesunden oder bei unvollständigen bzw. kompensierten Gefäßverschlüssen — nur durch Muskelarbeit, nicht aber durch arterielle Drosselung voll auszuschöpfen.
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  • 5
    ISSN: 1432-1440
    Keywords: Intravenous nitroglycerin ; Acute myocardial infarction ; Untreated control group ; Late intervention ; CK and CK-MB infarct-size ; Intravenöses Nitroglycerin ; akuter Herzinfarkt ; nicht behandelte Kontrollgruppe ; späte Intervention ; CK- und CK-MB Infarktgröße
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 38 Patienten mit frischem Herzinfarkt wurde die Wirkung von Nitroglycerin auf die Infarktgröße untersucht. Nach Randomisierung erhielten 16 Patienten eine Nitroglycerin-Dauerinfusion über 48 h in einer Dosierung zwischen 0,6 und 6,0 mg/h, im Mittel 2,3 mg/h. 22 Patienten blieben ohne spezifische Therapie und dienten als Kontrollgruppe. Die Intervention erfolgte im Mittel 12±5 (±1 SD) Stunden nach Beginn der Schmerzsymptomatik und 8±5 h nach Beginn des CK-Anstieges. Die Infarktgröße wurde aus dem Aktivitäts-Zeitverlauf der Creatinkinase (CK) und des myokardialen Isoenzyms der CK (CK-MB) bestimmt. Mit einer Ausnahme wurden bei allen Patienten gleichzeitig die hämodynamischen Parameter (linksventrikulärer Füllungsdruck, arterieller Blutdruck, Herzminutenvolumen) gemessen. Das mittlere Infarktgewicht in der Kontrollgruppe betrug 51±30 g, in der Nitroglyceringruppe 48±33 g. Das aus der CK-MB errechnete Infarktgewicht betrug in der Kontrollgruppe 60±36 g (n=16) und im behandelten Kollektiv 52±41 g (n=11). Bei einem linksventrikulären Füllungsdruck (LVFP) unter 20 mm Hg betrug das Infarktgewicht in der Kontrollgruppe 43±30 g (n=12), in der Nitroglyceringruppe 41±32 g (n=11). Bei einem LVFP über 20 mm Hg betrug das Infarktgewicht in der Kontrollgruppe 61±29 g (n=10) gegenüber 64±32 g (n=5) in der mit Nitroglycerin behandelten Gruppe. Auch bei der aus den ersten 7 h vorausberechneten Infarktgröße ergab sich zur beobachteten Infarktgröße kein Unterschied. Trotz der bekannten günstigen Wirkung von Nitroglycerin auf Hämodynamik und myokardiale Ischämie nahm das Infarktgewicht nur geringfügig ab. Dabei ist jedoch zu berücksichtigen, daß der Interventionszeitpunkt relativ spät war (12 h). Bei Frühintervention scheint eine günstige Beeinflussung möglich zu sein.
    Notes: Summary In 38 patients with acute myocardial infarction the effect of nitroglycerin on infarct size was studied. Patients were randomized into two groups. 16 patients received continuous nitroglycerin infusions of 0.6 to 6.0 mg/h (mean 2.3 mg/h) over a 48 h period, 22 patients received no specific therapy and served as control. Nitroglycerin was given in the mean 12±5 (±1 SD) hours following onset of chest pain and 8±5 h after the increase of CK values. Infarct size was determined according to the time activity curve of creatine kinase (CK) and of its myocardial isoenzyme (CK-MB). In all but one patient hemodynamic parameters (left ventricular filling pressure, blood pressure, cardiac index) were measured. The mean infarct size was 51±30 CK-g-equiv. in control patients, and 48±33 g in nitroglycerin treated patients. Infarct size as calculated from CK-MB values was 60±36 g (n=16) in control, and 52±41 g (n=11) in treated patients. At left ventricular filling pressure values (LVFP) below 20 mm Hg infarct size amounted to 43±30 g (n=12) in control, and to 41±32 g (n=11) in the nitroglycerin group. At LVFP values above 20 mmHg infarct size was 61±29 g (n=10) in control as opposed to 64±32 g (n=5) in treated patients. There was no difference between infarct size as predicted during the first 7 h and the observed infarct size. - Despite the known beneficial effect of nitroglycerin on hemodynamics and on myocardial ischemia, infarct size seems not to be greatly reduced, however, intervention occurred fairly late (12 h). In early intervention beneficial effects seem likely.
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  • 6
    ISSN: 1432-1041
    Keywords: captopril ; congestive heart failure ; plasma aldosterone ; plasma prolactin ; metoclopramide ; dexamethasone suppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary After long-term captopril treatment, an inappropriate increase in aldosterone levels has been observed in hypertensive patients. It is not known, whether a similar change would occur in patients with severe congestive heart failure, and whether it is due to a decrease in endogenous dopaminergic inhibition of aldosterone secretion or to aldosterone stimulation by ACTH or an ACTH-related peptide. Therefore, the aldosterone and prolactin responses to metoclopramide have been studied in 10 patients with severe congestive heart failure (NYHA Class III or IV) after 6 months of captopril treatment, before and 11 h after pretreatment with dexamethasone. 7 placebo-treated patients served as double-blind controls. In captopril-treated patients, the supine aldosterone levels exceeded the normal range and were as high as in placebo-treated patients. The responsiveness of aldosterone and prolactin to metoclopramide was not influenced by captopril. Only in the placebo group were the aldosterone levels decreased by dexamethasone. Captopril increased plasma renin activity and serum potassium, and decreased supine epinephrine and norepinephrine and serum sodium. Thus, previous reports of inappropriately high aldosterone levels after long-term captopril treatment were confirmed in patients with severe congestive heart failure. It is concluded that increased aldosterone is due neither to a decrease in endogenous dopaminergic inhibition nor to dexamethasone-suppressible stimulation of aldosterone secretion.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 38 (1990), S. S122 
    ISSN: 1432-1041
    Keywords: carvedilol ; propranolol ; coronary blood flow ; beta-blockade ; vasodilation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary A total of 17 patients with angiographically proven coronary artery disease and at least one stenosis blocking ≥ 70% of the left anterior descending or circumflex artery were included in a double-blind, randomized study. They received either 5 mg carvedilol or 6 mg propranolol intravenously. Heart rate, aortic pressure, mean coronary sinus pressure and coronary flow (thermodilution) were measured and coronary resistance and the rate-pressure product were calculated before and 25 min after injection. Carvedilol significantly (P 〈 0.05) lowered the heart rate (mean, 76 to 69 beats/min), aortic pressure (mean, 153/80–135/72 mmHg), rate-pressure product (mean, 117–93 mmHg/min), and coronary flow (mean, 114–94 ml/min). Coronary resistance (mean, 0.97–1.07 mmHg × min/ml) and coronary flow related to the rate-pressure product (mean, 1.0–1.02 ml/mm Hg) showed no significant change after carvedilol treatment. Propranolol lowered the heart rate (mean, 76–64/min;P 〈 0.05) and rate-pressure product (mean, 109–96 mm. Hg/min; not significant). Aortic pressure (mean, 145/72–147/74 mmHg), coronary flow (mean 109–101 ml/min), coronary resistance (mean, 1.1–1.2 mmHg × min/ml), and coronary flow related to the rate-pressure product (mean,1.12–1.19 ml/mmHg) showed no significant change after propranolol administration. Following single application, carvedilol lowered the rate-pressure product more markedly than did propranolol on account of its acute blood-pressure-lowering effect. No differences in the hemodynamic effects of carvedilol and propranolol were found. Neither drug seems to influence the adaption of coronary flow to myocardial oxygen demand.
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  • 8
    ISSN: 1432-1041
    Keywords: Isosorbide dinitrate ; Isosorbide-5-mononitrate ; Isosorbide-2-mononitrate ; muscle concentration ; vein wall concentration ; coronary bypass surgery ; drug distribution ; plasma concentration
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary The concentrations of isosorbide dinitrate (ISDN), isosorbide-5-mononitrate (IS-5-MN) and isosorbide-2-mononitrate (IS-2-MN) were determined in plasma (PL), saphenous vein wall (SV) and pectoral muscle (PM) from 8 patients undergoing coronary bypass surgery. The patients were pretreated for 2 days with ISDN 240 mg per day (standard release formulation) in 4 doses of 40 mg and one dose of 80 mg. The plasma and tissue samples were obtained during the operation, 10–12 h after the last dose. Isosorbide-2-mononitrate and isosorbide-5-mononitrate were present in plasma and tissues in the same concentration ranges with molar concentration ratios of 0.88 (IS-2-MN: PM/PL), 0.85 (IS-5-MN: PM/PL), 0.99 (IS-2-MN: SV/PL) and 1.06 (IS-5-MN: SV/PL). Mean ISDN concentrations in tissue were considerably higher than in plasma; the molar concentration ratios were 4.9 (SM/PL) and 7.21 (SV/PL). The accumulation of ISDN in vessel walls may contribute to its greater vascular action compared to the mononitrates, but it may also facilitate the development of tolerance during long-term treatment.
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  • 9
    ISSN: 1432-1041
    Keywords: Calcium channel blockers ; coronary atherosclerosis ; verapamil ; bypass surgery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Development of atherosclerotic lesions in animals, preferrably induced by a high-cholesterol diet, can be successfully suppressed by calcium channel blockers such as verapamil, nifedipine, nicardipine and diltiazem. The issue of a beneficial effect of calcium channel blockers on human coronary atherosclerosis is however not yet settled. At present, three prospective randomized clinical trials with calcium channel blockers (Nifedipine, Verapamil, Nicardipine) are being conducted (INTACT, FIPS, Study of theMontreal Heart Institute). Target variable for assessment of progression in these studies is the severity of coronary atherosclerosis evaluated by angiography both at entry into the study and after 2–3 years of treatment. A total of 445 patients after coronary bypass surgery (CABG) were entered in FIPS (Frankfurt Isoptin Progression Study) and randomly allocated to either verapamil 120 mg t. i. d. or placebo. The extent of coronary atherosclerosis is assessed by repeat angiography both 1 year and 3 years after randomization. Three vessel regions are evaluated separately: 1. Native vessels without bypass grafts and segments distal to the peripheral graft anastomosis (“core region”) 2. Segments bridged by bypass grafts and 3. Bypass grafts. The 1-year follow-up was completed by 162 patients (Group A = 80 patients; Group B = 82 patients). There was a homogeneous distribution in the two groups for all clinical variables, graft patency rates, and the incidence of clinical events (myocardial infarction, need for cardiac surgery or PTCA, cardiac death). The overall progression rate of atherosclerosis in the first year was expectedly low. Thus, the question of whether calcium channel blockers can retard the progression of coronary atherosclerosis will be answered after completion of the prospective trials. The analysis of the data of these studies must take into account that the natural history of coronary atherosclerosis is characterized by slow progression over time.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Medicine 41 (1990), S. 75-83 
    ISSN: 0066-4219
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Medicine
    Type of Medium: Electronic Resource
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