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Biomedical subjects

B Wüsten

Publications and source records attributed to B Wüsten.

At least 19 recordsLinked to original sources
PubMed2005

Long term adherence to dietary recommendations after inpatient rehabilitation: prospective follow up study of patients with coronary heart disease.

OBJECTIVE: To evaluate the adherence to nutritional recommendations in inpatient rehabilitation and the long term maintenance of dietary changes among patients with coronary heart disease. DESIGN: Prospective cohort study. SETTING: Two rehabilitation clinics in Germany. PARTICIPANTS: A cohort of 1206 patients undergoing inpatient rehabilitation after an acute manifestation of coronary heart disease. MAIN OUTCOME MEASURES: Self reported dietary intake before, during, and one and three years after rehabilitation measured with a semiquantitative food frequency questionnaire and summarised to a nutritional index, which was used to categorise patients as having a poor, fair, or good diet. RESULTS: During rehabilitation the proportion of patients whose dietary intake was categorised as good increased strongly from 30% to 91%. One and three years after rehabilitation a still increased proportion of 49% and 42%, respectively, in the good category was observed. The strong increase in intake of low fat and wholemeal products that was achieved during rehabilitation was followed after rehabilitation discharge by a backslide to the intake observed before rehabilitation admission. The avoidance of unfavourable food items, such as French fries or eggs, was at least partly maintained during the follow up period. CONCLUSION: During inpatient rehabilitation most patients do have to make major changes in their dietary intake to comply with recommendations. Although some proportion of patients continue to adhere to dietary recommendations in the long run, further research into strategies to improve maintenance of dietary changes is needed to enhance further the long term benefits from cardiac rehabilitation.

Adult↗
PubMed2003

[Changes of risk factors in patients with coronary heart disease after in-patient rehabilitation].

BACKGROUND AND OBJECTIVE: Rehabilitation therapy of patients with coronary heart disease (CHD) aims at reducing cardiovascular risk factors and at maintaining reduced risk factor levels. The aim of this analysis was to assess to what degree current in-patient rehabilitation and subsequent out-patient care by general practitioners (GPs) achieve these goals. PATIENTS AND METHODS: As part of the KAROLA-Study (Langzeiterfolge der KARdiOLogischen Anschlussheilbehandlung = Long-term success of cardiological rehabilitation therapy) 1206 patients between 30 and 70 years of age (mean age: male: 58.3 years, female: 60.8 years) who underwent in-patient rehabilitation due to CHD between January 1999 and May 2000 were recruited. Risk factor levels were assessed at the beginning and at the end of in-patient rehabilitation, and patients were re-examined one year after discharge using a standardised exam conducted by the GPs. RESULTS: Patients with increased risk factor levels at the time of admission showed significant improvements in the following risk factors during rehabilitation: Body mass index (-0.7 kg/m(2)), diastolic blood pressure (-10 mmHg), systolic blood pressure (-10 mmHg), total cholesterol (-73 mg/dl), LDL-cholesterol (-63 mg/dl), HDL-cholesterol (+ 3 mg/dl), triglycerides (-70 mg/dl). One year after discharge, however, all but one of the parameters (LDL-cholesterol) had re-increased significantly. The prescription of lipid lowering drugs rose from 56 % to 76 % during rehabilitation therapy and remained constant during the first year after discharge. CONCLUSIONS: During in-patient rehabilitation therapy important risk factors of CHD improved on average, but these improvements are only partly sustained in the long term. To ensure long-term success of rehabilitation measures more effective maintenance of risk factor modification in subsequent out-patient care is needed.

Adult↗
PubMed1986

Increase in number and decrease in size of mitochondrial profiles in myocytes of the right ventricle of dogs with experimental emphysema.

An ultrastructural study of the myocardium in control dogs and in dogs with papain-induced emphysema of 6 months duration without signs of right ventricular hypertrophy was undertaken to determine the number, size, and relative volume of the mitochondria. In the right ventricle of the emphysematous dogs, the number of mitochondrial profiles was greater per unit area of tissue (46.18 +/- 1.28/100 micron 2 versus 41.20 +/- 1.60/100 micron 2, p less than 0.05), but the mitochondria were smaller in size (mean mitochondrial profile area: 0.39 +/- 0.01 micron 2 versus 0.46 +/- 0.02 micron 2, p less than 0.05; mean mitochondrial "diameter": 0.65 +/- 0.01 micron versus 0.71 +/- 0.02 micron, p less than 0.05) than in control dogs. A highly significant negative correlation was found in the right ventricle of control and emphysematous dogs between the number per unit area and the size (area) of the mitochondrial profiles (r = -0.92; p less than 0.001). The increase in number but decrease in size of the mitochondrial profiles resulted in an unchanged relative volume of mitochondria in the right ventricle of the emphysematous dogs. In the subendocardium and in the subepicardium of the left ventricle of the papain-treated dogs, these changes were smaller and did not reach significance. These ultrastructural changes in the myocardium of the emphysematous animals are considered to be a response to a situation of prolonged increase in work of the right ventricle and may represent an early stage of a developing right ventricular hypertrophy.

Animals↗
PubMed1984

Increased myocardial capillary density in dogs with experimental emphysema.

In the hearts of control beagle dogs, capillary density in the right ventricle was found to be similar to that of the subendocardium of the left ventricle but lower than that of the subepicardium of the left ventricle. In emphysematous animals, 6 months after the exposure to papain (the emphysema-inducing agent), capillary density in the right ventricle and in the subendocardium of the left ventricle increased significantly, reaching values similar to that of the subepicardium of the left ventricle, which remained constant. These morphologic changes are considered to be an adaptation to a prolonged condition of increased myocardial oxygen demand and/or may represent an early stage of a developing cardiac hypertrophy.

Animals↗
PubMed1982

A six-month study of the evolution of papain-induced emphysema in the dog.

The development of papain-induced emphysema and the effect of structural changes of the lung on pulmonary hemodynamics were investigated in the dog in a 6-month study. Papain was administered as an aerosol at the beginning of the study and at Day 21; control animals received saline. At 3 or at 6 months, hemodynamic investigations were carried out in the awake animal (sedated with piritramide). The dogs were then killed and the lungs processed for morphometric evaluation. Arterial blood gases were analyzed at regular intervals for the duration of the study. In the papain-treated dogs, mean linear intercept (Lm) and internal surface area of the lungs corrected to an arbitrary lung volume of 2L (ISA2) were significantly different from control dogs both at 3 and at 6 months. No progression of the structural changes of the lung occurred between these two time intervals. Arterial blood oxygenation was normal throughout the study. In the papain-treated group at 6, but not at 3, months, mean pulmonary arterial blood pressure (PAPm) and pulmonary arteriolar resistance (PAR) were significantly augmented when compared with the control group. A significant correlation was found at 6 months between the Lm and ISA2 on one side, and PAPm and PAR on the other side, suggesting that the structural changes of the lung were responsible for pulmonary hemodynamic alterations.

Aerosols↗
PubMed1977

Role of cardiac contractility in hypertrophy from chronic volume loading.

In an experimental model of chronic cardiac volume overloading, ie chronic A-V block, evaluations of cardiac function were performed during the phase of the development of hypertrophy (one and two weeks of A-V block) and at stable hypertrophy (ten weeks of A-V block). During a time period of ten weeks of volume overload left ventricular muscle mass increased to 1.41 of normal hearts. Cardiac performance measured from cardiac index, stroke volume, and left ventricular ejection fraction was not depressed at any evaluated state of hypertrophy. Normal cardiac performance was also demonstrated when the heart was stressed by high ventricular pacing rates. The contractile state of the intact heart was expressed as the velocity of the isometric left ventricular pressure rise (dP/dt) at comparable loading conditions. Increased dP/dtmax at a stage before stable hypertrophy was reached, even when preload is normalised by ventricular pacing (70/min) implies that the volume overloaded heart during the development of hypertrophy mobilises part of its contractile reserve. It is assumed that increased contractility is a functional cause of an increase in oxygen demand; and that an adequate energy availability is covered by the enlargement of the mitochondrial mass. At stable hypertrophy when the contractile material has also increased, a new steady state is reached and an again normal contractility indicates an also stable dynamic situation.

Animals↗
PubMed1976

Quantification of collateral resistance in acute and chronic experimental coronary occlusion in the dog.

The resistance to coronary blood flow in various parts of the myocardium was studied with the tracer microspheres technique before and immediately after an acute coronary occlusion and several weeks after a more slowly occurring coronary occlusion by Ameroid constrictor. All experiments were carried out in the isolated, metabolically supported, empty, beating dog heart at maximal coronary vasodilation induced with adenosine. Coronary resistance of the normal empty beating heart at maximal coronary vasodilation was 0.20 mm mm Hg/(ml/min) per 100 g of tissue (subepicardium) and 0.16 mm Hg/(ml/min) per 100 g of tissue (subendocardium). After acute coronary occlusion the perfusion of the subtended myocardium was maintained at a much lower level by way of collateral vessels, which showed a resistance to flow of 3.52 mm Hg/(ml/min) per 100 g. If coronary artery occlusion proceeded more slowly the collateral vessels became more functional and myocardial infarction was avoided. During collateral enlargement collateral resistance fell from 3.52 to 0.22 mm Hg/(ml/min) per 100 g within a period of 8 weeks after implantation of the constricting device. The degree of compensation by collaterals for the loss of the occluded native coronary artery was 33% of its former conductance.

Acute Disease↗
PubMed1975

Influence of perfusion pressure and heart rate on local myocardial flow in the collateralized heart with chronic coronary occlusion.

We studied the influence of controlled changes in perfusion pressure and heart rate on the regional distribution of myocardial flow in normal dogs and in dogs with multiple chronic coronary artery occlusions but without infarctions. Local myocardial blood flow was determined with the tracer microsphere technique. By stepwise altering of systemic blood pressure during maximal vasodilation classical pressure flow relations were obtained. One week after complete chronic occlusion a functionally and anatomically well-defined compartmentation of blood flow was found. The dilatory reserve is clearly compromised not only in the collateral-dependent myocardium but also in the apparently normal myocardium which delivers collateral flow. An "arterio-arterial shunting" mechanism is shown to exist. Several months after coronary occlusion, regional mycoardial flow is still nonhomogeneous. Although the coronary dilatory capacity of the collateralized myocardium is nearly normal, that of the normal myocardium is found to be higher than normal. Vessel growth in both areas is discussed as being responsible for this phenomenon. Right ventricular pacing during maximal vasodilation produces a flow decrease to the endocardial muscle layers in normal dogs, while the epicardial flow is unchanged. One week after complete chronic coronary occlusion pacing during maximal vasocilation reduces the dilatory capacity in the collateralized areas to such an extent that the supplementary increase in myocardial oxygen demand will induce ischemia because of the compromised oxygen supply.

Animals↗
PubMed1975

Effects of prindolol on isoproterenol-induced subendocardial ischaemia in dogs with multiple chronic coronary artery occlusion.

Multiple chronic coronary artery occlusions were produced in dogs by implantation of ameroid rings on the circumflex branches of the left and right coronary artery. Sixty-five per cent of the animals survived. Seventy-seven per cent of the remaining animals had no detectable myocardial infarction. Myocardial blood flow distribution was studied 4 weeks after operation using the tracer microsphere technique. During control conditions myocardial blood flow was homogeneously distributed within the left ventricle. In one group of dogs, regional dilatory capacity was tested by intravenous infusion of dipyridamole. Four compartments of myocardial blood flow were found. The collateral dependent subendocardium with 114 ml/min-100 g-1 was the lowest perfusion rate. In another group of dogs myocardial blood flow distribution was examined during isoproterenol infusion and after beta-blockade with prindolol during continuous isoproterenol infusion. During isoproterenol infusion, a nonhomogeneous blood flow pattern was found when the heart rate increased to 200/min together with a slight fall in diastolic perfusion pressure. Under these conditions, the flow to the collateral dependent subendocardium was severely diminished, while the flow to the areas perfused by normal coronary arteries increased, reflecting compensatory vasodilation. After beta-blockade with prindolol 0.1 mg/kg, the myocardial blood flow distribution was also nonhomogeneous but in the opposite direction: the collateral dependent subendocardium was now the best perfused compartment. The flow to the areas perfused by normal coronary arteries decreased due to the reduced oxygen requirements, while the collateral dependent subendocardium remained maximally dilated. This phenomenon was explained as a postischaemic reactive hyperaemic response to the isoproterenol-induced ischaemia in the collateral dependent subendocardium.

Animals↗