[Causal therapy in chronic heart failure].
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Biomedical subjects
Publications and source records attributed to B Höfling.
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In 22 patients we studied the effects of 0.2 mg nifedipine given intracoronary during the course of routine PTCA. In 9 patients the effect of the nifedipine-free solvent was additionally tested. Injections were made through the guiding catheters or balloon catheters as pre- and poststenotic injections. We monitored frequency and character of pain, ECG changes (continuous recording of full 12-lead ECG) and pressure recordings from the left ventricle and pre- and poststenotic coronary artery. Short-lasting "stinging" pain sensations were described by 41% of the patients after nifedipine and 33% after solvent injection (n.s.). Patients described the pain as different from their usual angina pectoris. Pain was more frequent after poststenotic injections (through the balloon catheter) than after pre-stenotic injections (59% vs. 19%, p less than 0.01). ECG changes were peaking T waves, ST elevation and ST depression. They were recorded after pre-stenotic injections in 21 of 22 cases for nifedipine and 6 of 9 for solvent and after poststenotic injections in 22 of 22 cases for nifedipine and 8 of 9 cases for solvent. After nifedipine 0.2 mg i.c. the pressures decreased by 3.5% pre-stenotic and 9.7% post-stenotic. LVEDP increased by 10.7%. Our results show that pain sensations and electrocardiographic changes occur with similar character and frequency after i.c. injections of nifedipine or nifedipine-free solvent. Thus these effects do not seem to be caused by nifedipine. Hemodynamic effects were small and there was no disproportionate decrease of poststenotic pressure.
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Transient ischaemic ST segment changes were studied in 296 consecutive patients with coronary heart disease attending hospital for coronary arteriography. They underwent two channel, frequency modulated ambulatory monitoring for 24 hours. During this time 221 episodes of transient ST elevation (n = 56) or ST depression (n = 165) with a horizontal deviation of at least 1 mm lasting at least 1 min were found in 70 patients (23.6%). Only 34% of episodes were associated with pain. The duration of the episode, the heart rate at the beginning of the episode, or the extent of ST deviation were not related to the occurrence of pain. Episodes of ST elevation were of significantly shorter duration, occurred significantly more often during the early morning, and at significantly lower heart rates than episodes of ST depression. The considerable overlap between the characteristics of episodes of ST elevation and ST depression suggests that in many instances a combination of factors is responsible for transient ischaemic ST segment changes.
Coronary heart disease and end-stage renal disease: Coronary heart disease is frequent in patients with end-stage renal disease. Without invasive procedures coronary heart disease is often not diagnosed in patients with end-stage renal disease. We have no evidence for accelerated progression of coronary heart disease under conditions of dialysis. Valvular heart disease and end-stage renal disease: Valvular heart disease shows an increasing frequency depending on the period of dialysis. Valvular heart disease is often unnoticed and constantly underestimated without invasive investigation. Valvular heart disease often indicates a bad prognosis in our patients with end-stage renal disease.
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Coronary artery perforation is a rare but potentially lethal complication during percutaneous transluminal coronary angioplasty (PTCA). To avoid pericardial tamponade, it has been suggested that perforating wires or balloons should not be withdrawn and that the patient should be transferred immediately to surgery. We report a case with a perforating and broken intracoronary guide wire which was successfully extracted using a Dotter intravascular retriever catheter. The only consequence was a small pericardial effusion not requiring pericardial puncture. Thus, emergency surgery is not inevitable after coronary artery perforation caused by thin intracoronary guide wires.
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We investigated the toxicity of adriamycin (ADM) in dogs with regard to autologous bone marrow transplantation (BMT). Gastrointestinal toxicity limited the dose of ADM in single administration (3.0 mg/kg) and chronic cardiotoxicity in repeated administration (9 X 1.5 mg/kg every two weeks). The recovery of hemopoiesis was complete within 25 days after single and repeated doses of ADM as indicated by the restoration of blood counts and concentration of hemopoietic precursors (CFUc) as well as proliferate activity of bone marrow. At this time bone marrow was obtained and reinfused after total body irradiation (TBI) with 10 Gy. Single and repeated doses of 1.5 mg/kg ADM did not delay recovery of blood counts after autologous BMT as compared to transplantation of untreated marrow - in contrast a single dose of 3.0 mg/kg ADM did. Our results indicate that toxicity of ADM is not influenced by autologous BMT. Previous shorter therapy with conventional doses of ADM does not preclude autologous BMT.
Muscle-mechanical and hemodynamic properties were measured in adriamycin-treated rats and in untreated controls. The respective parameters in both animal groups could not be distinguished at rest. Using a pharmacological stress test with dobutamine a differentiation of both groups was possible: the concentration-response curve of papillary muscles from ADM-rats was lower and shifted towards higher concentrations when compared with the respective curve of untreated animals. The maximum hemodynamic response following an i.v. bolus injection of dobutamine was considerably decreased in ADM-rats as compared to untreated rats. It is concluded that the estimation of impaired myocardial function due to adriamycin might be more accurate when the contraction reserve is evaluated.
The muscle mechanical and haemodynamic effects of adriamycin were investigated in guinea pigs and rats by use of isolated myocardium (isometric contractions of papillary muscles of guinea pigs and rats) and in situ preparations (haemodynamic parameters in thoracotomized rats). 1. Adriamycin (10-6 to 10-3 M) produced a concentration-dependent negative inotropic effect in papillary muscles of 21 guinea pigs (decrease of T max and dT/dt max to 80% of control) and in papillary muscles of 15 rats (decrease of T max and dT/dt max to 25% of control for maximally effective concentrations). 2. The haemodynamic parameters left ventricular pressure (LVP), dLVP/dt max, arterial pressure and cardiac output of thoracotomized rats (N = 12) decreased dose-dependently following i.v. injections of adriamycin at doses of 2-30 mg/kg until a lethal haemodynamic shock occurred. 3. "Low-dose-effects" were reversible within min, whereas "high-dose-effects" were not up to an observation period of 1 h. 4. In the haemodynamic experiments, the ionized serum calcium fell excessively after adriamycin (from 2.1 mEq/l for controls to 0.5 mEq/l after doses of 25 mg/kg adriamycin). 5. An antagonistic interaction was seen between the cardio-depressant effect of adriamycin and the positive inotropic effect of calcium and vice versa. 6. It is concluded that the acute muscle mechanical and haemodynamic effects of adriamycin result from an interaction between adriamycin and calcium.
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The myocardial contents of DNA, protein, total and polyribosomal RNA, messenger RNA (mRNA) and polyribosomes were determined in normal and adriamycin-treated rats. While the myocardial contents of DNA and protein changed only little in adriamycin-treated rats, total and polyribosomal RNA decreased by 23.2% and 35%, mRNA and polyribosomes by 51.6% and 38.7%. Size distribution and protein synthetic activity of the polyribosome preparations obtained remained unchanged in the adriamycin-treated rats. We conclude that the reduced myocardial contents of RNA, mRNA and polyribosomes cause the previously observed impairment of myocardial protein synthesis in adriamycin-treated rats and might be important in the pathogenesis of the adriamycin-cardiomyopathy.
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The effects of changes in viscosity on pressure flow relations in the in situ perfused left circumflex coronary artery were studied in open chest dogs. Vascular reactivity was abolished by maximal pharmacological coronary dilatation. Blood and suspensions of red cells (hematocrit 8-14%) in dextran solutions were used as perfusates. Total perfusion energy dissipation, represented by perfusion pressure drop across the perfused vascular bed, can be separated into a viscous and an inertial fraction: P = Pvisc + Pinert. Perfusing the heart with approximately Newtonian fluids of different viscosities enabled us to compute the amount of the inertial fraction of total perfusion pressure dissipation. At constant viscosity, the inertial fraction increased with flow rate. However, the rise of the inertial fraction due to reduced viscosity at a constant perfusion pressure was much more pronounced. Variations of perfusion pressure and viscosity of the perfusates between 70 to 130 mm Hg and 1.2-3.2 cP, respectively, resulted in inertial perfusion pressure dissipation between 16 and 54%. This inertial pressure drop may become a noteworthy factor under conditions of low whole blood viscosity (e.g. anemia or therapeutical hemodilution.
Coronary flow and myocardial oxygen consumption were measured in conscious dogs at rest and during two levels of submaximal treadmill exercise (3 and 7 km/h at 15% grade, respectively) during adaptation to progressive hemodilution with dextran 60. At rest coronary flow increased to more than seven-fold with diminishing hematocrit to 12.5% in order to cover myocardial oxygen consumption which increased from 6.5 +/- 0.3 ml/min with 100 g at hematocrit 47.5% to 13.5 +/- 0.8 ml/min with 100 g at hematocrit 12.5%. The dilatory capacity of the coronary vessels, estimated from the reactive hyperemia after a 12 sec occlusion of the left circumflex coronary artery, dropped from 602% at control to 45% at lowest hematocrit levels. During the superimposed stress of exercise coronary flow and myocardial oxygen consumption increased further, so that the dilatory capacity of the coronaries was exhausted at hematocrit levels between 16 and 22%. Myocardial oxygen consumption per unit of oxygen delivered to peripheral tissues increased substantially with progressive hemodilution. In the presence of the reduced arterial oxygen content the augmented myocardial oxygen demand limits the overall adaptability to hemodilution by an exhaustion of the coronary dilatory capacity.