H. Klepzig

Noninvasive assessment of left ventricular performance following transluminal coronary angioplasty.

We studied 36 patients with successful transluminal coronary angioplasty (group 1) noninvasively using exercise electrocardiography, exercise T1-201 myocardial scintigraphy and equilibrium radionuclide ventriculography before and 3-5 days after the procedure. Six patients who underwent aortocoronary-bypass surgery (group 2) and 10 patients with stable angina pectoris (group 3) served as controls. All patients had arteriographically documented coronary artery disease at least in one major coronary vessel (stenosis greater than or equal to 70%). In group 1, average coronary stenosis was 81.1 +/- 8.4% before dilatation and 44 +/- 13.7% after the procedure (P less than 0.001). Ischemia score in the exercise electrocardiography decreased from 2.4 +/- 2.7 before dilatation to 0.4 +/- 0.8 after the procedure (P less than 0.001). Myocardial perfusion in computerized T1-201 myocardial scintigraphy 5-10 min after exercise expressed as vitality index (the ratio of T1-201 uptake in the ischemic region to the region of maximal uptake in the same image analyzed carefully in the same view in 2 studies) increased from 72.9 +/- 8.4% before dilatation to 79.9 +/- 11.7% after the procedure (P less than 0.001). Ejection fraction at rest increased from 47.2 +/- 9.2% to 51.0 +/- 9.7% (P less than 0.001) and during exercise from 39.9 +/- 10.5% to 49.4 +/- 10.9% (P less than 0.001) before and after the procedure. In group 2, noninvasive studies showed a tendency to improvement after surgery. In group 3 no significant changes were noted. We conclude that transluminal coronary angioplasty improves both coronary perfusion to ischemic areas supplied by critical coronary artery stenoses and left ventricular function, especially during exercise, if luminal diameter is dilated by greater than 20%.

Effect of atenolol and celiprolol on acetylcholine-induced coronary vasomotion in coronary artery disease ☆

Earlier studies have reported on the potentiated muscarinic vasoconstriction of intracoronary acetylcholine after metoprolol application in patients with coronary artery disease. The present study investigated the effect of celiprolol, atenolol, and placebo on acetylcholine-induced vasomotion in patients with coronary artery disease. Furthermore, direct effects on coronary vasomotion and on hemodynamics were evaluated. Acetylcholine (intracoronary concentrations of 6.3x10(-7), 2.0x10(-6), and 6.3x10(-6) M) was given before and after double-blind celiprolol (0.30 mg/kg IV), atenolol (0.15 mg/kg IV), or placebo in 3x12 patients. Vasomotion was investigated by quantitative coronary angiography in proximal and distal segments of epicardial coronary arteries, and by the determination of the coronary resistance index based on Doppler-flow measurements. The investigated drugs had no direct affect on the diameter of the epicardial coronary arteries. However, celiprolol, in contrast to atenolol, significantly reduced systemic vascular resistance (change after atenolol: from 1,855+/-308 to 2,161+/-550 dyne s cm(-5); celiprolol: 1,691+/-435 to 1,411+/-343 dyne s cm(-5); and placebo: 1,722+/-215 to 1,710+/-213 dyne s cm(-5), p<0.001) and the coronary resistance index (change after atenolol: 2.52+/-3.58 to 2.86+/-4.24; celiprolol: 2.70+/-1.55 to 2.49+/-2.26; and placebo: 1.97+/-1.35 to 1.92+/-1.25, p<0.01). Celiprolol, atenolol, and placebo did not have different effects on acetylcholine-induced coronary vasomotion of epicardial conductance vessels (diminution of proximal lumen diameter before/after atenolol: 0.42+/-0.39/0.44+/-0.39 mm; celiprolol: 0.32+/-0.26/0.30+/-0.24 mm; and placebo: 0.36+/-0.29/0.43+/-0.40 mm) and of coronary resistance vessels (reduction of coronary resistance index before/after atenolol: 1.95 +/-4.74/ 1.92+/-3.74; celiprolol: 0.98+/-0.73/1.41+/-1.50; and placebo: 1.16+/-1.29/1.16+/-1.04). In contrast to atenolol, celiprolol possesses vasodilative properties in systemic and coronary resistance vessels. There was no direct effect on the diameter of conductance vessels. Acetylcholine-induced coronary vasomotion both in conductance and resistance vessels was not influenced by the beta blockers that were studied. This suggests that atenolol and celiprolol do not influence endothelium-dependent, nitric oxide related vasomotion.

Effect of propranolol and disopyramide on left ventricular function at rest and during exercise in hypertrophic cardiomyopathy.

In 19 patients with hypertrophic cardiomyopathy (15 males, 4 females, mean age 49.2 ± 10.8 years) left ventricular function was studied with radionuclide ventriculography at rest and during exercise i

Combined first-pass and equilibrium radionuclide ventriculography and comparison with left ventricular/right ventricular stroke count ratio in mitral and aortic regurgitation

Effective and total left ventricular (LV) stroke volume were assessed in 31 patients with verified aortic or mitral regurgitation, or both, and in 22 patients with normal valvular function using combined first-pass and equilibrium radionuclide ventriculography. The difference between these 2 volumes as a fraction of LV stroke volume was taken as the radionuclide regurgitant fraction. The results were compared with the LV/right ventricular (RV) stroke count ratio and with the angiographic regurgitant fraction according to the method of Sandler and Dodge. Radionuclide regurgitant fraction derived from 2 determinations with a time interval of 1 week showed good reproducibility (n = 15, r = 0.96, SEE = 9.1). Sensitivity was 100% for radionuclide regurgitant fraction and 87% for LV/RV stroke count ratio at equal specificity (100%). Radionuclide regurgitant fraction was more sensitive, especially in severely ill patients, in whom additional RV volume overload led to false-low or false-negative ratios. Angiographic and radionuclide regurgitant fraction showed linear correlation (r = 0.79, p less than 0.001). In contrast, because 5 patients had RV volume overload, only a weak correlation could be noticed between angiography and LV/RV stroke count ratio (r = 0.47, p less than 0.05). Excluding these patients, correlation substantially improved (r = 0.74, p less than 0.001). The combination of first-pass and equilibrium radionuclide ventriculography is a sensitive, specific and well reproducible method for the evaluation of mitral and aortic regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Extracellular matrix structure after heart transplantation

Following heart transplantation remodeling of the donor heart causes changes in the extracellular myocardial matrix. We investigated 20 right ventricular endomyocardial biopsies taken 17+/-4 days (group I, n=9) and 63+/-13 days (group II, n=11) after heart transplantation from 16 patients transplanted for end-stage cardiomyopathy (15 dilated/1 ischemic). Immunohistochemical staining for collagen I, collagen III, collagen IV, and fibronectin was used. Evaluation was performed at a magnification of 400x using a computer-assisted image analyzing system measuring the relative area stained by the immunoperoxidase method, the number of cells in the given area, and the total area. Collagen I per cell was 13.9+/-5.9 microm2 in group I and increased significantly 66+/-13 days after heart transplantation in the perimysium around the myocardial cells as well as in the endocardium to 49.9+/-15.1 microm2 (P<0.05). No quantitative change in collagen III was noted (75.7+/-12.4 versus 75.5+/-16.0 microm2 n.s.). Collagen IV was found in the perimysial, in the capillary bed and in the vascular network. Significant quantitative change in the amount of collagen IV was not found (64.1+/-12.6 versus 61.0+/-8.9 microm2). Fibronectin was found in the entire perimysial extracellular matrix and in the endocardium in relationship with collagen I and III. An increased amount of fibronectin from 87.09+/-9.9 microm2 (group I) to 140.8+/-17.9 microm2 (group II, P<0.05) was found. The cell area and cell diameters were not significantly different (group I; cell area 772+/-227 microm2, diameter 31.3 microm; group II; cell area 776+/-224 microm2, diameter 31.4 microm). It is concluded that remodeling of the donor heart after transplantation is characterized by a specific increase in collagen I and fibronectin, whereas a change in other collagen subtypes was not observed.

Hemodynamic effects of nitroglycerin in an experimental model of acute aortic regurgitation

Afterload reduction is an accepted therapeutic modality for the treatment of congestive heart failure caused by chronic aortic regurgitation. However, the role of vasodilator therapy in acute aortic incompetence has not been established. To investigate this, left ventricular volume overload was produced in 18 dogs by constructing a valved conduit from the descending thoracic aorta to the left ventricular apex. The time course of aortic, pulmonary and conduit flows was analyzed in eight control studies and established stability of the experimental model. In the remaining 10 dogs, intravenous nitroglycerin, titrated to reduce mean aortic blood pressure by 40%, and placebo (ethanol) were each infused for 20 min periods. Compared with placebo, nitroglycerin significantly reduced aortic flow (3,945 +/- 324 to 3,397 +/- 362 ml/min, p less than 0.01), regurgitant flow (1,304 +/- 131 to 764 +/- 90 ml/min, p less than 0.001), septal-lateral end-diastolic diameter (47.5 +/- 1.8 to 46.5 +/- 1.8 mm, p less than 0.001), left ventricular end-diastolic pressure (6.9 +/- 0.8 to 6.0 +/- 0.6 mm Hg, p less than 0.05), left ventricular stroke work (19.0 +/- 2.6 to 10.8 +/- 1.7 g-m/beat, p less than 0.001) and systemic vascular resistance (2,253 +/- 173 to 1,433 +/- 117 dyne-s/cm5, p less than 0.001). In contrast, pulmonary flow, left anterior descending coronary flow and subendocardial pH did not change during infusion of either nitroglycerin or placebo. These data indicate that by decreasing preload and afterload, and by preserving coronary flow and tissue pH, nitroglycerin effectively reduced ventricular and regurgitant volumes in the setting of acute volume overload.(ABSTRACT TRUNCATED AT 250 WORDS)

Protective action of hydroxyethyl rutosides on singlet oxygen challenged cardiomyocytes

1 The effect of a standardized mixture of β‐hydroxyethyl rutosides against oxidative damage in singlet oxygen‐challenged isolated cardiac myocytes from adult rats was investigated. The morphology of the myocytes was evaluated as an indicator for cell viability (elongated, rod shaped cells vs. hypercontracted, rounded cells). The determination of the production of thiobarbituric acid reactive substances served as an indicator for lipid peroxidation. 2 Exposure to singlet oxygen which was generated by photo‐excitation of rose bengal (10−7 m) reduced the number of rod shaped (vital) cardiomyocytes by 78.5 ± 2.5% and increased the production of thiobarbituric acid reactive substances by 1180 ± 150% in comparison to incubation with control buffer. 3 Coincubation of the cells with β‐hydroxyethyl rutosides (concentration range: 6.7 pg ml−1 to 670 μg ml−1) increased the number of rod shaped cardiomyocytes after exposure to singlet oxygen in a dose‐dependent bell‐shaped manner. A significant protective effect was observed at β‐hydroxyethyl rutosides concentrations ranging from 0.67 ng ml−1 to 67 ng ml−1. 4 In spite of their protective action, β‐hydroxyethyl rutosides did not reduce the accumulation of thiobarbituric acid reactive substances, used as an indicator for lipid peroxidation. 5 The data suggest that β‐hydroxyethyl rutosides exert a protective action against oxygen radical‐induced damage of cardiac myocytes at very low concentrations without interfering with lipid peroxidation.

Effect of propranolol and disopyramide on left ventricular function at rest and during exercise in hypertrophic cardiomyopathy

In 19 patients with hypertrophic cardiomyopathy (15 males, 4 females, mean age 49.2 +/- 10.8 years) left ventricular function was studied with radionuclide ventriculography at rest and during exercise in a crossover design without intervention and after disopyramide and propranolol treatment. 15 of the 19 patients had a resting or latent intraventricular gradient of more than 30 mm Hg. Left ventricular function at rest and during exercise was evaluated before medication, 90 min after oral administration of 200 mg disopyramide or 160 mg propranolol and after 3 weeks of oral therapy with disopyramide 200 mg 2 times a day or propranolol 80 mg 4 times a day. After long-term treatment with disopyramide, resting ejection fraction decreased from 72 +/- 12 to 69 +/- 14% (p less than 0.01) and peak ejection rate (PER) decreased from 3.46 +/- 135 to 3.24 +/- 65 end-diastolic volume (EDV).s-1 (p less than 0.01). Peak filling rate (PFR) at rest decreased from 3.01 +/- 0.8 to 2.77 +/- 0.63 EDV.s-1 (p less than 0.05). Time to peak filling rate (TPFR) at rest and during exercise after acute and chronic therapy did not change compared to control values. Acute and long-term administration of propranolol lead to a significant reduction in heart rate at rest and during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial Function Before and After Transluminal Coronary Angioplasty

In selected cases transluminal coronary angioplasty (TCA) may represent an effective alternative to bypass surgery in the treatment of coronary heart disease [2, 3, 4, 9, 15].

Neue experimentelle Untersuchungen zum Mechanismus der Ballondilatation

Die transluminale koronare Angioplastik mittels Ballonkatheter nach Gruntzig wird in zunehmendem Mase erfolgreich bei Patienten mit koronarer Herzkrankheit eingesetzt. Zur Klarung der durch den Eingriff verursachten histologischen Veranderungen sind von verschiedenen Autoren tierexperimentelle Prufungen und Versuche an Leichenherzen durchgefuhrt worden. Ziel der hier vorgestellten Arbeit war, den Einflus einer simulierten Dilatation auf die Morphologie und das Gewicht von Arterien frisch Verstorbener zu untersuchen.