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B Schwartzkopff

Publications and source records attributed to B Schwartzkopff.

At least 37 records · Page 2Linked to original sources

[Duplex ultrasound risk stratification of percutaneous puncture of the brachial artery for diagnostic and interventional coronary angiography].

Diagnostic and interventional heart catheterization in peripheral vascular disease often requires due to iliacal disease additional methods of arterial approach besides the Judkin's technique. The percutaneous catheterization of the brachial artery finds widespread use. A major complication linked with this method is an increased rate of thrombotic occlusions at the puncture site. Thus, we investigated in a prospective set-up the ability of duplex ultrasound to identify predictive risk factors for vascular complications. Over a period of 20 months, 8000 patients referred to heart catheterization were studied. Routine catheterization via the femoral route was contraindicated in 34 out of 8000 mostly due to severe peripheral vascular disease with multiple vascular risk factors (diabetes, hypertension, and smoking). 53 patients who had a comparable low risk-profile served as the control group. The brachial artery was examined by ultrasound duplex for vessel anatomy and diameter at the puncture site before coronary angiography. Both groups (patient and control group) showed in 15% a variable anatomy with a premature division of the brachial artery in 6% proximal of the elbow and in 9% already distal to the axillary artery. Because of reduced diameters of these variable vessels no procedure was carried out at these arms. In all cases the opposite arm was successfully used instead, because the variants were always located only at one arm. The diameter of the brachial artery measured in average 5.0 +/- 0.8 mm and 4.8 +/- 0.7 mm in patients and controls, respectively. Women had a significantly smaller vessel diameter than men, measuring a difference of 0.4 and 0.6 mm, respectively (p < 0.05). For coronary angiography 6F and 7F arterial sheats were used equally, and in 32% of all cases a coronary intervention was performed. 31 (91%) procedures were carried out without complications; there was a false aneurysm in 1 patient (3%) and an occlusion of the brachial artery at the puncture site in 2 patients (6%). The occluded vessels of two diabetic women had a reduced diameter at the level of 10% of the standard distribution and an unfavorable ratio of sheat-to-vessel-diameter which lead initially to an obstruction of nearly 50% of the vessel lumen during catheterization. Screening of the brachial artery by ultrasound duplex before a percutaneous catheterization for coronary angiography and intervention showed reproducibly the variable anatomy and differences in vessel diameter, which can be risk factors for thrombotic occlusion. Important details for the location of the puncture site and the possible size of the arterial sheat can be obtained, so that coronary interventions with 7F catheter systems are still practicable. This technique is a simple and efficient method to estimate the relative risk of arterial occlusion prior to percutaneous puncture of the brachial artery, especially in a group of patients with severe atherosclerosis and elevated vascular risk-factors.

Adult↗

Evidence of endothelial dysfunction of epicardial coronary arteries in patients with immunohistochemically proven myocarditis.

BACKGROUND: Recent reports indicate that myocarditis can be associated with acute myocardial ischemia and even myocardial infarction in patients with normal arteriograms. We therefore tested the hypothesis that patients with biopsy-proven myocarditis have endothelial dysfunction despite angiographically smooth epicardial coronary arteries. METHODS AND RESULTS: Graded concentrations of the endothelium-dependent vasodilator acetylcholine (10(-6) to 10(-4) mol/L) and for comparison, the non-endothelium-dependent vasodilator nitroglycerin (0.3 mg intracoronary), were infused into the left coronary arteries of 18 patients (mean age 47+/-9 years, 8 women and 10 men) with biopsy-proven myocarditis but without angiographically demonstrable coronary artery disease. Vascular responses were analyzed by quantitative coronary angiography. Three patients had an intact vasodilator response to acetylcholine concentrations of up to 10(-4) mol/L in all segments of the left coronary artery, with a mean dilatation of +9.9%+/-2%. In contrast, paradoxical constriction by acetylcholine occurred in 9 patients, who showed a mean change in coronary artery diameter of - 11%+/-3%. Six patients had no significant change in any segments in response to acetylcholine (-2.5%+/-4%). There was a significant inverse correlation between the number of T-lymphocytes in the myocardium and the response of the epicardial coronary arteries to acetylcholine (Pearson correlation coefficient -0.49, P=.03). CONCLUSIONS: It can be assumed that the process of myocarditis is associated with impairment of endothelium-dependent vasodilation in response to acetylcholine in most patients. Vasoconstriction in the presence of acetylcholine in myocarditis is likely to reflect an abnormality of endothelial function. Endothelial dysfunction of coronary arteries may explain the occurrence of myocardial ischemia in patients with myocarditis.

Acetylcholine↗

Alterations of the architecture of subendocardial arterioles in patients with hypertrophic cardiomyopathy and impaired coronary vasodilator reserve: a possible cause for myocardial ischemia.

OBJECTIVES: The study was designed to investigate the architecture of subendocardial arterioles of patients with hypertrophic cardiomyopathy (HCM) and angina pectoris with respect to coronary vasodilator reserve. BACKGROUND: There is growing evidence that the coronary microvasculature is abnormal in HCM. Arterioles, which mainly regulate intramyocardial blood flow, are especially suspect. METHODS: Thirteen patients with HCM (50.1+/-12.6 years old, mean value +/- SD) were studied after exclusion of any relevant coronary stenoses. Subendocardial arterioles (density [n/mm2], wall area [microm2], percent lumen area [%lumen], periarteriolar collagen area [microm2]), myocyte diameter (microm) and interstitial collagen fraction (Vv%) were evaluated by means of stereologic morphometry of transvenous biopsy samples. Coronary blood flow was measured quantitatively with the inert chromatographic argon method at basal conditions and after dipyridamole (0.5 mg/kg body weight over 4 min intravenously), and coronary vasodilator reserve was calculated as the ratio of coronary resistance at basal conditions and after pharmacologic vasodilation. Data from five normotensive subjects (45.4+/-11 years old, p = NS) served as control data. RESULTS: Arteriolar density was diminished by 38% (p = 0.004) and %lumen by 13% (p = 0.009) in patients with HCM compared with control subjects. Coronary reserve was impaired in patients with HCM (2.28+/-0.6 vs. 5.34+/-1.49, p = 0.003) because of higher coronary resistance after vasodilation (0.48+/-0.14 vs. 0.22+/-0.06 mm Hg x min x 100 g/ml, p = 0.004). Coronary vasodilator reserve correlated with arteriolar density (r = +0.47, p = 0.045) and with %lumen (r = 0.65, p = 0.003). CONCLUSIONS: In HCM, the architecture of preterminal subendocardial arterioles is altered by a reduced total cross-sectional lumen area, corresponding to an impaired coronary vasodilator capacity that may predispose to myocardial ischemia.

Adult↗

What is the value of home (self) blood pressure monitoring in patients with hypertensive heart disease?

The acceptable maximal blood pressure values for patients monitoring their own blood pressure at home have not yet been determined. Risk of cardiovascular disease may be increased at lower blood pressure limits than those suggested by the World Health Organization (WHO) for clinic readings. We have investigated 25 patients with proven hypertensive small-vessel disease and compared self-monitored, ambulatory 24-h (ABPM) and clinic blood pressure measurements. The diagnosis of hypertensive small-vessel disease was based on clinical evidence of myocardial ischemia, angiographic exclusion of coronary heart disease, and abnormal single-photon emission computed tomography (SPECT) thallium-201 myocardial scintigraphy. Mean self-monitored values were 143.4 +/- 13.6/84.0 +/- 9.4 mm Hg (95% confidence intervals 137.6-149.0 mm Hg for systolic and 80.1-87.9 mm Hg for diastolic blood pressure). Both home and ambulatory daytime readings (141.2 +/- 11.8/83.9 +/- 10.2 mm Hg) were significantly lower than the clinic readings by the physicians (clinic systolic, 169.2 +/- 16.5 mg; clinic diastolic, 95.0 +/- 11.6 mm Hg; P < .0001 v home and ambulatory readings). There was no significant difference between home and ambulatory readings. Agreement between home and ambulatory values was much closer than for clinic v ABPM readings. The respective correlation coefficients for systolic values were r = 0.702 (home v ABPM; P < .0001) and r = 0.32 (clinic v ABPM; NS). For diastolic values correlation coefficients were r = 0.674 (home v ABPM; P < .0002) and r = 0.574 (clinic v ABPM; P < .003) respectively. In conclusion, the reported results suggest that the WHO suggested definition of hypertension (> or = 140/90 mm Hg) may be set too high when blood pressures are measured by the patient at home. A cutoff value of < 135/85 mm Hg, as in ABPM, may be a more realistic upper limit for self-monitoring.

Aged↗

Objectives of high blood pressure treatment: left ventricular hypertrophy, diastolic function, and coronary reserve.

The prehypertrophic state of hypertensive heart disease is characterized by morphologic changes (interstitial fibrosis, increase in intramyocardial arteriolar wall thickness) as well as by functional alterations (diastolic dysfunction, decrease in coronary reserve). These changes most probably represent the earliest cardiac end-organ lesions that can clinically be detected. In cardiac hypertrophy, long-term (9-12 months) pharmacotherapy with beta-blockers, calcium channel blockers, or ACE inhibitors reverses left ventricular hypertrophy by 8% to 14%, whereas marked improvement in coronary reserve and diastolic dysfunction is achieved by calcium blocker and preferably by ACE inhibitors.

Antihypertensive Agents↗

Immunohistochemical video-microdensitometry of myocardial collagen type I and type III.

Collagen is an essential part of the cardiac interstitium. Collagen subtypes, their location, total amount and the architecture of the fibrillar network are of functional importance. Architecture in terms of density of the fibrillar network is assumed to be reflected by the intensity of immunohistochemical staining of collagen. The aim of this study was to evaluate a video-based microdensitometric method for quantifying density expressed as absorbance of collagen subtypes I and III stained with an indirect immunoperoxidase method in myectomy specimens of patients with hypertrophic obstructive cardiomyopathy. Various factors influencing the immunohistochemical staining product and the technical properties of the image analysis system were investigated. Linearity between collagen concentration and the absorbance of the immunohistochemical staining product was demonstrated for collagen I using a dot-blot technique. Immunohistochemical collagen staining and density measurement were easily reproducible. The cardiac disability of the patients was assessed according to the New York Heart Association (NYHA) criteria. There was a significant increase in collagen type I density with higher NYHA class, whereas no significant association was found for total collagen area fraction. Thus, video-based microdensitometry gives further insight into the structural remodelling of myocardial collagens and reveals their significance in the process of heart failure in hypertrophic cardiomyopathy.

Adolescent↗

Assessing the coronary circulation in hypertension.

Systemic arterial hypertension is one of the major risk factors for coronary artery disease, coronary microangiopathy, and left ventricular hypertrophy, all of which can potentially lead to cardiac failure and sudden cardiac death. Coronary flow reserve is defined as the maximal increase in coronary flow above its resting, autoregulated level for a given perfusion pressure. In arterial hypertension functional and structural alterations are observed at the level of epicardial vessels as well as in resistive vessels requiring sophisticated approaches to assess coronary flow reserve and thus myocardial perfusion. Electrocardiographic tests and echocardiography can be regarded as monitoring and screening methods. Myocardial scintography is useful to semiquantitatively estimate hypertension-associated perfusion abnormalities, whereas positron emission tomography provides the only quantitative approach of a non-invasive technique for myocardial blood flow measurement. Invasive methods for the assessment of coronary blood flow need cardiac catheterization procedures, such as techniques requiring catheterization of the coronary sinus, angiographic methods, and guidewire based methods. Thermodilution and venous oxymetry in the coronary sinus systematically underestimate coronary flow reserve and are thus considered as only semiquantitative approaches. In contrast, the gas chromatographic argon method allows a quantitative measurement of coronary blood flow at baseline and during maximum vasodilation; thus it is possible to distinguish between an altered autoregulated and maximal flow as the major cause of a reduced coronary flow reserve and to evaluate long-term therapeutic interventions in hypertensive hearts. Videodensitometric and angiographic methods should be restricted only to patients with coronary microangiopathy or with coronary single-vessel disease. Guidewire-based Doppler techniques are suitable to semiquantitatively assess coronary flow reserve with a considerable spatial and time resolution. Myocardial biopsies may gain insight into hypertension-associated structural alterations in small arterioles. Long-term treatment of hypertensive heart disease aims to normalize blood pressure, to reduce left ventricular hypertrophy and to achieve cardioreparation including reversal of the abnormal structure and function of coronary circulation. Based on the different methods for assessment of coronary circulation the therapeutic value of different classes of antihypertensive therapeutics will be evaluated in this overview.

Animals↗

[Early postoperative changes in systolic and diastolic function at rest and during stress in patients with hypertrophic obstructive cardiomyopathy (HOCM) after myectomy].

INTRODUCTION: In this study systolic and diastolic function in patients with hypertrophic obstructive cardiomyopathy (HOCM) and intractable complaints to medication were investigated before and after a mean of 7 months after myectomy. METHODS: Investigations in 19 patients with HOCM included echocardiography, Swan-Ganz-thermodilution-catheter and radionuclide-angiography. RESULTS: Myectomy resulted in a reduction of the intraventricular gradient at rest (40.1 +/- 43.3 versus 7.6 +/- 12.0 mm Hg, p < or = 0.005) and under provocation (92.4 +/- 67.1 versus 21.3 +/- 26.5 mm Hg, p < or = 0.001). Echocardiographically determined basal septal thickness was reduced (24.9 +/- 6.3 versus 20.1 +/- 6.8 mm; p < or = 0.05) and diastolic diameter increased (40.4 +/- 5.2 versus 44.8 +/- 7.1; p < or = 0.05). Exercise tolerance increased from the maximally achieved 64.5 +/- 19.2 to 89.5 +/- 24.0 W (p < or = 0.001). Symptomatic status (NYHA) improved (1.7 +/- 1.4 versus 2.8 +/- 0.3 (p < or = 0.001). Systolic parameters showed at rest an increase in isovolumetric contraction time (65 +/- 39 versus 112 +/- 50 ms, p < or = 0.01), in time to peak ejection (109 +/- 40 versus 188 +/- 42 ms, p < or = 0.001), and a reduced left ventricular ejection fraction (72 +/- 12 versus 64 +/- 11%, p < or = 0.01). Analysis of regional ejection fraction revealed a significant reduction of ejection fraction in the basal septal region (p < or = 0.05). Increase of global and regional ejection fraction under exercise was still preserved. Mean pulmonary capillary wedge pressure was significantly reduced at rest (11.8 +/- 3.8 versus 8.6 +/- 2.4 mm Hg, p < or = 0.05) as well as under exercise (27.0 +/- 7.1 versus 20.4 +/- 6.8 mm Hg, p < or = 0.01), whereas left ventricular enddiastolic volume index (63 +/- 19 versus 72 +/- 17 ml*m-2, p < or = 0.05) was significantly increased. CONCLUSIONS: In patients with HOCM, myectomy reduces intraventricular gradient, increases exercise capacity, and is accompanied by improved diastolic function parameters, while systolic function parameters are generally reduced.

Adult↗

[Intracoronary dipyridamole reduces the incidence of acute coronary vessel occlusion in percutaneous transluminal coronary angioplasty--a prospective randomized study].

Even in the era of coronary stenting, acute coronary artery occlusion continues to represent a significant limitation of percutaneous transluminal coronary angioplasty (PTCA). Despite application of heparin and aspirin, abrupt vessel closure still occurs in 2-8%, depending on the definition applied. Especially patients receiving PTCA for acute coronary syndromes are at high risk for abrupt vessel closure. The formation of an intracoronary thrombus plays a central role in the pathogenesis of abrupt vessel closure. Dipyridamole induces dilatation of coronary arteries and prevents platelet aggregation by a mechanism that differs from that of aspirin. The primary purpose of the study was to evaluate whether adjunctive local intracoronary therapy with dipyridamole could reduce the incidence of coronary artery occlusion following PTCA. Secondary endpoints were defined as myocardial infarction, necessity for bypass grafting, and death. In 939 PTCA procedures performed for stable angina and in 155 angioplasty procedures for acute coronary syndromes (unstable angina, acute myocardial infarction), patients were randomized to receive conventional pretreatment consisting of heparin 15,000 I.E. and aspirin 500 mg i.v. or additional intracoronary infusion of dipyridamole (0.5 mg/kg body weight). Dipyridamole was applied in 550 interventions (455 interventions in men, 95 interventions in women, age = 59.2 +/- 8.4; 74 emergency procedures); conventional pretreatment was performed in 544 interventions (444 interventions in men, 100 interventions in women, age 58.3 +/- 7.9; 81 emergency procedures). Intracoronary application of dipyridamole resulted in a significant reduction in the incidence of abrupt vessel closure following PTCA. This significant reduction was observed in patients presenting with stable ischemia as well as in patients receiving PTCA for acute coronary syndromes. Concerning secondary end points, intracoronary application of dipyridamole did not affect the need for bypass grafting or the incidence of death following PTCA. Intracoronary application of dipyridamole was associated with a reduction in the incidence of myocardial infarction following PTCA which, however, failed to reach significance.

Adult↗

Structural analysis of arteriolar and myocardial remodelling in the subendocardial region of patients with hypertensive heart disease and hypertrophic cardiomyopathy.

Left ventricular hypertrophy is a risk factor for cardiovascular morbidity and mortality. In arterial hypertension and in hypertrophic cardiomyopathy it may be accompanied by clinical signs of myocardial ischaemia resulting from microcirculatory dysfunction in the absence of coronary macroangiopathy. Structural changes of the vascular and interstitial compartment of the heart are involved in the pathogenesis of impaired microcirculation. We investigated patients with hypertensive heart disease (HHD; n = 12) and hypertrophic cardiomyopathy (HCM; n = 19) without coronary macroangiopathy but with signs of myocardial ischaemia. Right septal endomyocardial biopsies were evaluated to quantify the structure of intramyocardial arterioles, collagen content and myocytic diameter by morphometric rules. Nine normotensive subjects served as controls. The groups differed significantly (P < 0.05) in myocytic diameter and total collagen content. The myocytic diameter correlated with the thickness of the interventricular septum. Arterioles in HHD showed a significant increase in cross-sectional medial area and in HHD patients the periarteriolar collagen area increased both in absolute terms and when standardized to medial area. Arteriolar density was significantly reduced in HCM. In a multivariate discriminant analysis the positive predictive value for differentiation of the groups by non-myocytic variables was 72.5% (P = 0.013). HHD and HCM differ in the structural alterations in the arteriolar bed. Medial hypertrophy and periarteriolar fibrosis prevail in HHD, and reduced arteriolar density is found in HCM. Different microvascular remodelling at the level of arterioles indicates distinct pathophysiologic processes that may contribute to the clinically observed disturbance of coronary microperfusion in these two diseases.

Adult↗

Evidence for reduced coronary flow reserve in patients with insulin-dependent diabetes. A possible cause for diabetic heart disease in man.

UNLABELLED: In diabetic heart disease myocardial, interstitial, coronary and neural structures are often involved. Coronary microangiopathy is supposed to contribute an essential part, which has not yet been clearly analysed. METHODS: In 9 normotensive patients with insulin-treated diabetes (DP) with clinically suspected coronary heart disease but normal epicardial coronary arteries, coronary microcirculation was studied. Coronary flow was determined as the quotient of base line and minimal coronary resistance after dipyridamole (0.5 mg/kg i.v.), using the argon-gas-chromatography method. Systolic left ventricular function was analysed by ventriculography, diastolic function by M-Mode-echocardiography and Doppler-echocardiograhy. Twelve normotensive subjects served as control group (CON). RESULTS: In diabetic patients maximal coronary flow was significantly reduced (172 +/- 5 versus 395 +/- 103 ml/min x 100 g, p < or = 0.001) and minimal coronary resistance increased (0.6 +/- 0.19 versus 0.24 +/- 0.06 mmHg x min x 100 g/ml, p < 0.001). Coronary reserve in diabetics was markedly reduced (1.84 +/- 0.39 versus 4.23 +/- 0.52, p < or = 0.001). Global systolic function was normal in all patients (EF: DP: 72 +/- 13 versus CON: 77 +/- 12%, n.s.; cardiac index: DP: 3.2 +/- 0.8 versus CON: 3.3 +/- 1.2 1/ min x m2, n.s.). Diastolic function was impaired in diabetics with an increased relaxation time index (97 +/- 23 versus 45 +/- 18 msec, p < or = 0.01) and an impaired diastolic inflow pattern, indicated by the E/A-ratio (0.75 +/- 0.14 versus 1.66 +/- 0.13, p < or = 0.05). CONCLUSIONS: The reduced coronary flow reserve in patients with insulin-treated diabetes mellitus may play a crucial role in the pathophysiology of diabetic cardiopathy, causing myocardial ischaemia due to a disturbance of coronary microcirculation leading to diastolic dysfunction and progressing assumably to systolic failure.

Cholesterol↗

Impaired coronary flow reserve in NIDDM: a possible role for diabetic cardiopathy in humans.

Diabetic cardiopathy represents a cardiac disorder with involvement of myocardial, interstitial, coronary, and neural structures. One of the main manifestations refers to coronary microangiopathy, which has not yet been clearly identified. Coronary hemodynamics, including the determination of coronary flow reserve, were therefore analyzed in normal subjects and in nine patients with NIDDM and clinically suspected coronary heart disease but normal coronary arteriogram. Coronary flow reserve was determined as the quotient of baseline and minimal coronary resistance after dipyridamole (0.5 mg/kg i.v.). Coronary blood flow was measured quantitatively by the argon method. Systolic left ventricular function was analyzed by ventriculography and diastolic function by M-mode and Doppler echocardiography. Twelve healthy normotensive subjects served as the control group (CON). In the diabetic patients, maximal coronary flow was significantly reduced (172 +/- 50 vs. 395 +/- 103 ml/min x 100 g; P < 0.001), and minimal coronary resistance was increased (0.60 +/- 0.19 vs. 0.24 +/- 0.06 mmHg x min x 100 g/ml; P < 0.001). Coronary reserve in the diabetic subjects was markedly reduced (1.84 +/- 0.39 vs. 4.23 +/- 0.52; P < 0.001). No difference existed with respect to myocardial oxygen consumption (12.4 +/- 2.3 vs. 11.8 +/- 2.8 ml O2/100 g x min; NS). Global systolic function was normal in all patients (ejection fraction: NIDDM 72 +/- 13 vs. CON 77 +/- 12%, NS; CI: NIDDM 3.2 +/- 0.8 vs. CON 3.3 +/- 1.2 l/min x m2, NS). Diastolic function was impaired in diabetic patients with an increase in relaxation time index (97 +/- 23 vs. 45 +/- 18 ms; P < 0.01) and an impaired diastolic inflow pattern, indicated by the ratio between early and late transmitral flow (0.75 +/- 0.14 vs. 1.66 +/- 0.13; P < 0.05). We conclude that the markedly reduced coronary flow reserve in diabetic patients may play a key role in the induction and perpetuation of coronary insufficiency in myocardial ischemia, in diastolic and systolic dysfunction, and in the initiation of diabetic cardiopathy.

Aged↗

Left ventricular hypertrophy and coronary microcirculation in hypertensive heart disease.

Hypertensive heart disease is a major factor for left ventricular hypertrophy, the development of ischaemic syndromes, including coronary macro- and microangiopathy, and heart failure. Coronary microcirculation is impaired very early in the process of hypertensive heart disease, giving suspect that impaired coronary reserve is an early indicator for the conversion from the normal into the pathologic status. Alterations at the level of the interstitium with accumulation of collagen, of the intramyocardial resistance vessels with remodelling or hypertrophy of the vessel wall, of the endothelium with reduced vasodilators and increased vasoconstrictors as well as of the capillaries with a reduction in their numbers may all be involved in the process of the impaired coronary reserve. Therapeutic interventions by antihypertensive therapy can improve coronary reserve.

Coronary Circulation↗

Pharmacologic myocardial protection during percutaneous transluminal coronary angioplasty by intracoronary application of dipyridamole: impact on hemodynamic function and left ventricular performance.

OBJECTIVES: The aim of this study was to investigate whether intracoronary infusion of dipyridamole represents a suitable tool for preventing deterioration of left ventricular performance and hemodynamic function during percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Coronary angioplasty represents a suitable model for establishing myocardial ischemia in humans. Balloon inflation is usually accompanied by significant deterioration in left ventricular systolic and diastolic properties. A brief episode of ischemia followed by reperfusion, termed preconditioning, has been identified as a mechanism for rendering the myocardium more resistant to ischemia. Adenosine is considered an important mediator of preconditioning. Dipyridamole is an important drug that interferes with myocardial adenosine metabolism by inhibiting its cellular reuptake. METHODS: In 20 patients undergoing elective coronary angioplasty of a major vessel, assessment of angiographic left ventricular performance and hemodynamic variables was performed before, during and after PTCA. Patients were randomly allocated to pretreatment with intracoronary infusion of dipyridamole before percutaneous transluminal coronary angioplasty (10 patients) or conventional pretreatment without dipyridamole (10 patients). RESULTS: Dipyridamole pretreatment resulted in significant preservation of systolic and diastolic left ventricular performance during percutaneous transluminal coronary angioplasty, as documented by an unaffected global ejection fraction (vs. a deterioration of 29.2% with conventional pretreatment, p < 0.01) and an increment in diastolic stiffness of only 12.7% (vs. an increment of 57.3% with conventional pretreatment, p < 0.01). Apart from one instance of coronary steal phenomenon, no significant side effects of dipyridamole infusion could be detected. CONCLUSIONS: It is concluded that intracoronary application of dipyridamole may result in the induction of myocardial preconditioning by improving systolic and diastolic ventricular performance during percutaneous transluminal coronary angioplasty, thereby potentially reducing the risk of the angioplasty procedure.

Aged↗

Myocarditis--cardiomyopathy. Consensus Report of the German Association for Internal Medicine, presented at the 100th annual meeting, Wiesbaden, 13 April 1994.

On the basis of several, partially divergent definitions, myocarditis-unlike the often aetiologically unexplained (idiopathic) cardiomyopathies (dilated, hypertrophic, restrictive)-can be classified as c specific disease of the myocardium. This disease often has a known cause and can be due to a large variety of aetiological agents (viral, autoreactive, toxic, infectious processes, etc.) (1). A question still to be answered is whether there is a connection between dilated cardiomyopathy and myocarditis, i.e. whether (virus-induced) myocarditis can progress via a subacute or chronic stage to dilated cardiomyopathy. This question is of considerable diagnostic and therapeutic relevance. The following consensus report thus deals with the clinically important problems related to the diagnosis of myocarditis and dilated cardiomyopathy, examines the aetiological role of immunological mechanisms and discusses the treatment of the two diseases and prognostic factors.

Cardiomyopathy, Dilated↗