Hemodynamic effects of prenalterol in patients with ischemic heart disease and congestive cardiomyopathy.

Erbel, Raimund; Meyer, Jürgen; Lambertz, Heinz; Schweizer, P.; Voelker, Wolfram; Krebs, W.; Braun, Gustav; Effert, S

doi:10.1161/01.cir.66.2.361

Cited by 34 publications

(9 citation statements)

References 22 publications

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“…In contrast, others have treated cardiomyopathic patients with /3,-agonists, s u c n a s P rer >-alterol, and have demonstrated improvement in their clinical condition. 8 Thus, to date, there is not a consensus on the best treatment regimen for congestive cardiomyopathy.…”

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confidence: 99%

L-carnitine treatment improves cardiac performance and restores high-energy phosphate pools in cardiomyopathic Syrian hamster.

Whitmer

1987

Circulation Research

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Hamsters with either the dilated (BIO 53.58) or hypertrophic (BIO 14.6) form of cardiomyopathy and an inbred control strain of hamster (FIB) were treated for 6 months with high-dose L-carnitine (1 g/kg/day i.p.). After treatment, the animals were killed and their hearts perfused by the isolated working technique. Mechanical performance (as indicated by the double product of heart rate and left ventricular [LV] peak systolic pressure) of both carnitine-treated cardiomyopathic groups was increased significantly above their respective sham-treated groups. Associated with these increases in mechanical performance were significant increases in both peak-positive LV dP/dt (index of contractility) and peak negative dP/dt (index of relaxation) in both carnitine-treated myopathic groups. Serum carnitine levels were increased 10-15 times within 2 hours after injection of L-carnitine in all 3 groups. Myocardial free-carnitine levels were increased twofold in both control and dilated myopathic hearts above their respective sham-treated groups, restoring the level in the dilated hearts comparable to those of controls. Myocardial carnitine levels in the hypertrophic group were not significantly affected by treatment. Total high-energy phosphate stores, i.e., ATP plus creatine phosphate, were restored to control levels by L-carnitine treatment in both cardiomyopathic groups. Levels of the breakdown products of ATP were maintained primarily in the more readily convertible adenosine diphosphate and adenosine monophosphate forms in all three treated groups. These changes resulted in significantly higher ratios of (ATP)/(ADP + AMP + adenosine) and (creatine phosphate)/ (creatine) in the treated hearts. This is the first study demonstrating that high-dose L-carnitine treatment results in improved cardiac performance and increased myocardial total high-energy phosphate stores in the Syrian hamster model with one of two distinct forms of cardiomyopathy, i.e., dilated or hypertrophic. The mechanisms for these effects of exogenous L-carnitine treatment cannot be totally explained by changes in oxidative energy metabolism. (Circulation Research 1987; 61:396-408)

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confidence: 99%

L-carnitine treatment improves cardiac performance and restores high-energy phosphate pools in cardiomyopathic Syrian hamster.

Whitmer

1987

Circulation Research

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“…However, the changes were dependent on the initial hemodynamic condition. 12 In all our patients the hemo- dynamic and echocardiographic findings were decidedly poor. The congestive heart failure of the patients could not be sufficiently compensated with cardiac glycosides, diuretics, and vasodilators.…”

Section: Resultsmentioning

confidence: 67%

Long-term hemodynamic effects of prenalterol in patients with severe congestive heart failure.

Lambertz¹,

Meyer²,

Erbel³

1984

Circulation

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In a controlled, randomized, double-blind study we investigated the long-term effects of the PI -adrenoceptor agonist prenalterol in 16 patients with severe congestive heart failure (NYHA class III or IV). Previous to and 1 week, 3 months, and 6 months after continuous oral intake of 40 to 120 mg prenalterol a day, catheterization of the right heart combined with an ergometer test was carried out; M mode and two-dimensional echocardiograms as well as systolic time intervals were also recorded. With prenalterol the heart rate increased within 1 week from 81 ± 7 to 90 ± 7 beats/min (mean ± SD) (p < .05) and remained increased after 3 months (93 + 9 beats/min, p < .01) and 6 months (91 + 6 beats/min, p < .05). After 1 week the cardiac index rose from 2.7 + 0.7 to 3.3 + 0.7 1/min/m2 (p < .01), and after 3 and 6 months it fell again to 3.0 ± 0.9 1/min/m2 and 2.9 ± 0.7 1/min/ m2, respectively. In the ergometer test the improvement in performance was not significant. The mean velocity of circumferential fiber shortening initially increased from 0.58 + 0.20 to 0.79 ± 0.28 circumferences/sec (p < .01), but dropped after 3 months to 0.62 ± 0.31 circumferences/sec. The ejection fraction determined from the two-dimensional echocardiogram rose after 1 week from 20 + 10 to 27 + 12% (p < .05), but decreased again after 3 months (23 + 11%) and 6 months (20 ± 10%). Initially, the end-diastolic pressure of the pulmonary artery decreased from 24 ± 5 to 21 ± 6 mm Hg (p < .05), but rose again after 3 months to 23 + 6 mm Hg and after 6 months to 23 ± 4 mm Hg. After 1 week, the index for duration of the mechanical systole decreased by 3.8 + 2.3% (p < .001), but after 3 and 6 months such an improvement was no longer evident. The results indicate that prenalterol is not an effective drug for the treatment of patients with heart failure, because its effects are not sustained during long-term administration. Circulation 69, No. 2, 298-305, 1984. IN PATIENTS whose severe congestive heart failure cannot be sufficiently compensated with cardiac glycosides, diuretics, or vasodilators, the administration of a positive inotropic drug should be considered.iA The ,f3-adrenoceptor agonist prenalterol (the left isomeric form of S-(-)-1-(4-hydroxyphenoxy)-3-isopropylamino-2-propranolol-hydrochloride) can be given both intravenously and orally. In animal studies5 and clinical investigations, this substance was shown to have aB,/-stimulating property.-'7 It was the aim of this controlled, randomized, double-blind study to test the long-term effects after oral administration of prenalterol.

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“…Positive inoptropic interventions (dobutamine, isoproterenol, amrinone, nebivolol, prenaterol, exercise, Bay 5959, MS 857, OPC-18790) 24,25,30,37,41,[57][58][59][60][61][62][63][64][65][66][67][68][69][70][71] caused similar increases in OperCon, EF, Vcf and dP/dt-max, whereas elastance changes were significantly higher. Negative inotropic interventions (propranolol, intracoronary nifedipine, diltiazem, verapamil, ischaemia, chronic tachypacing, dilated cardiomyopathy, aortic regurgitation with ventricular dysfunction) 24,25,40,53,57,58,65,66,[72][73][74][75][76][77][78][79][80][81][82][83][84][85][86][87][88][89] caused comparable reductions in OperCon and other indices (Fig.…”

Section: Retrospective Evaluationmentioning

confidence: 95%

“…After exclusion of these articles, 67 studies were analysed, which contained data from load [44][45][46][47][48][49][50][51][52][53][54][55][56] and inotropic manipulations, 24,25,30,37,40,41,53, 38 in humans ( n = 687 subjects) and 29 in dogs ( n = 302 animals). All these articles reported their findings as mean values and 12 [34][35][36][37]40,46,52,64,68,75,83,84 further provided individual values for the relevant variables (11 in humans, one in dogs).…”

Section: Retrospective Datamentioning

confidence: 99%

Operative contractility: A functional concept of the inotropic state

Curiel

Perez-Gonzalez

Torres

et al. 2005

Clin Exp Pharma Physio

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1. Initial unsuccessful attempts to evaluate ventricular function in terms of the 'heart as a pump' led to focusing on the 'heart as a muscle' and to the concept of myocardial contractility. However, no clinically ideal index exists to assess the contractile state. The aim of the present study was to develop a mathematical model to assess cardiac contractility. 2. A tri-axial system was conceived for preload (PL), afterload (AL) and contractility, where stroke volume (SV) was represented as the volume of the tetrahedron. Based on this model, 'operative' contractility ('OperCon') was calculated from the readily measured values of PL, AL and SV. The model was tested retrospectively under a variety of different experimental and clinical conditions, in 71 studies in humans and 29 studies in dogs. A prospective echocardiographic study was performed in 143 consecutive subjects to evaluate the ability of the model to assess contractility when SV and PL were measured volumetrically (mL) or dimensionally (cm). 3. With inotropic interventions, OperCon changes were comparable to those of ejection fraction (EF), velocity of shortening (Vcf) and dP/dt-max. Only with positive inotropic interventions did elastance (Ees) show significantly larger changes. With load manipulations, OperCon showed significantly smaller changes than EF and Ees and comparable changes to Vcf and dP/dt-max. Values of OperCon were similar when AL was represented by systolic blood pressure or wall stress and when volumetric or dimensional values were used. 4. Operative contractility is a reliable, simple and versatile method to assess cardiac contractility.

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Hemodynamic effects of prenalterol in patients with ischemic heart disease and congestive cardiomyopathy.

Cited by 34 publications

References 22 publications

L-carnitine treatment improves cardiac performance and restores high-energy phosphate pools in cardiomyopathic Syrian hamster.

L-carnitine treatment improves cardiac performance and restores high-energy phosphate pools in cardiomyopathic Syrian hamster.

Long-term hemodynamic effects of prenalterol in patients with severe congestive heart failure.

Operative contractility: A functional concept of the inotropic state

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