Anamnese und klinischer Befund: Untersuchungen: Therapie und Verlauf: Folgerung: History and clinical findings: Investigations: Treatment and course: Conclusion:

History and clinical findings: A 54-year-old man was urgently admitted because of sudden onset of progressively worsening angina pectoris, his first attack. Physical examination was unremarkable.Investigations: Electrocardiography and laboratory tests excluded acute myocardial infarction. With the exception of hypercholesterolemia (toal cholesterol 247 mg/dl) laboratory tests were normal. Coronary angiography revealed a 60% eccentric narrowing in the proximal part of the interventricular branch with adjacent aneurysmatic dilatation. Intravascular ultrasound (IVUS) showed a coronary pseudoaneurysm, its cavity communicating with the empty atheroma hole of an adjacent ruptured coronary plaque.Treatment and course: A 19 mm stent graft was implanted, via a percutaneously inserted balloon-catheter system, in the region of the stenosis and the pseudoaneurysm. Subsequent angiography demonstrated a smooth nonstenotic lumen. The membrane of the graft (made of polytetrafluoroethylene [PTFE]), fixed between two thin metal stents, had occluded the pseudoaneurysm. Occlusion of an immediately distal septal branch briefly produced an asymptomatic rise of creatine kinase to maximally 173 U/l. Oral medication included ticlopidine hydrochloride (2 x 250 mg daily for 4 weeks). The patient was symptom-free after the procedure and was discharged 5 days later.Conclusion: Implantation of a new type of stent-graft provides quick and uncomplicated treatment of a coronary aneurysm. The membrane fixed between two stents prevents wash out of any thrombi. The method may also be applicable to other potentially thrombus-containing lesions.

In patients with congestive heart failure (CHF), overactivity of the sympathetic nervous system may be accompanied by an impairment of the baroreflex control mechanism. To evaluate the reflex responses of the sympathetic nervous system, the renin-angiotensin system and vasopressin release to baroreceptor unloading, 38 patients with left ventricular dysfunction were studied. Hemodynamic data, and plasma norepinephrine, renin activity and vasopressin concentrations were measured before and 60 minutes after administration of high-dose hydralazine (0.4 mg/kg intravenously). On the basis of blood pressure response to vasodilator administration, patients were divided arbitrarily into those with a decrease in mean arterial blood pressure ≥15 mm Hg (group A; n = 12) and those with a decrease <15 mm Hg (group B; n = 26) compared with control values. In response to hydralazine, heart rate decreased in group A from 100 to 92 beats/min (p < 0.001) and increased in group B from 90 to 96 beats/min (p < 0.05). In group A, hemodynamic changes induced by hydralazine were accompanied by a decrease in plasma norepinephrine from 822 to 518 pg/ml (p < 0.01) and an increase in plasma vasopressin from 8.4 to 45.2 pg/ml (p < 0.001). In group B, plasma norepinephrine and vasopressin did not change significantly (407 vs 447, and 8.4 vs 8.3 pg/ml, respectively). Plasma renin activity remained unchanged in group A and increased in group B (p < 0.001). The data show that baroreceptor-mediated release of vasopressin is not impaired in patients with CHF and a defective sympathetic reflex control mechanism. Thus, baroreceptor-mediated vasopressin release may represent a protective mechanism to maintain systemic blood pressure in a subgroup of patients with severe CHF.

Systemic and coronary haemodynamic effects of carbochromen (0.125 mg kg-1 min-1 for 40 min i.v.) and dipyridamole (0.05 mg kg-1 min-1 for 10 min i.v.) were investigated in 18 patients without detectable heart disease. Both drugs induced a comparable increase in coronary blood flow (carbochromen: from 82 +/- 23 to 337 +/- 68 ml.100 g-1.min-1; dipyridamole: from 78 +/- 9 to 301 +/- 61 ml.100 g-1.min-1). This resulted in a minimal coronary resistance of 0.23 +/- 0.04 mmHg.ml-1.100 g.min for dipyridamole and of 0.24 +/- 0.04 mmHg.ml-1.100 g.min for carbochromen. In response to dipyridamole (n = 12) heart rate increased from 73 to 94 beats min-1 (P less than 0.005) and mean aortic pressure fell from 89 to 78 mmHg (P less than 0.001). After administration of carbochromen (n = 6) no significant systemic effects occurred. Dipyridamole induced a significant increase in myocardial oxygen consumption by 46% (P less than 0.001); after application of carbochromen myocardial oxygen consumption remained unchanged. From these data it can be concluded that for the evaluation of coronary dilatory capacity carbochromen may be more suitable than dipyridamole because (1) maximal coronary vasodilation is induced without changes in myocardial oxygen consumption and (2) no systemic effects occur.

In patients with typical stress-induced anginal pain, normal coronary arteries, and unimpaired left ventricular performance at rest ("syndrome X"), a reduced coronary dilatory capacity, abnormal lactate metabolism during stress, and reduction of left ventricular functional reserve have been described. A group of 40 patients with syndrome X was followed for several years to determine their long-term prognosis. In 27 patients pulmonary artery pressure and in 19 patients left ventricular ejection fraction were reassessed during rest and exercise approximately 4 years after the initial examination. In patients with stress-induced ST-segment depression, these variables did not change during the observation period. In patients with constant or rate-dependent left bundle branch block, however, there was significant deterioration of left ventricular performance during rest (pulmonary artery mean pressure, 16 +/- 3 vs. 17 +/- 4 mm Hg, p = NS; left ventricular ejection fraction, 62 +/- 5% vs. 55 +/- 5%, p less than 0.05) and exercise (pulmonary artery, 30 +/- 6 vs. 39 +/- 10 mm Hg, p less than 0.005; left ventricular ejection fraction, 59 +/- 6% vs. 49 +/- 5%, p less than 0.01). These findings suggest that in syndrome X two subgroups with distinctly different prognoses may be defined: In patients with stress-induced ST-segment depression during exercise, left ventricular performance remains well preserved; however, in patients with either constant or rate-dependent left bundle branch block, there is significant deterioration of left ventricular function within several years.

Patients with syndrome X have an appreciable reduction in coronary reserve, i.e. the dilatory capacity of the coronary resistance vessels. Whereas the intramyocardial vessels are normal, there are degenerative changes in myocardial cells, shown on electron microscopy. Left ventricular function is normal under resting conditions but becomes abnormal during isometric or dynamic stress. The diagnosis of syndrome X is predominantly based on a marked reduction in coronary reserve. Furthermore, delayed T1-wash out and increased glutamate turnover have been observed. Follow-up studies reveal some heterogeneity of patients studied; in patients with syndrome X and left bundle branch block left ventricular function deteriorates progressively.

The pathogenesis of angina pectoris in patients with left ventricular hypertrophy secondary to arterial hypertension and with normal coronary arteries remains uncertain. We measured coronary blood flow (argon method) in 12 control subjects and in 16 patients with arterial hypertension at rest and after intravenous administration of dipyridamole (0.5 mg/kg). In the patients with arterial hypertension, coronary blood flow response to dipyridamole was markedly reduced (p less than .001 as compared with control values). During coronary vasodilation there was a linear correlation between coronary resistance and left ventricular end-diastolic pressure (r = .67, p less than .001). Left ventricular catheter biopsy specimens did not reveal alterations in myocardial microvasculature. These findings suggest that reduction of coronary reserve may be an important contributor to the pathogenesis of angina pectoris in these patients.

In conventional myocardial Thallium-201 scintigraphy, regional myocardial Thallium-201 activity is compared to the area of normal, i.e., maximal activity. In the presence of multivessel coronary artery disease, this mode of evaluation may yield false negative results. -In 87 patients suffering from coronary artery disease and in 26 controls, after simultaneous i.v. injection of Thallium-201 and Technetium-99m coronary transit times of Thallium-201 were determined as the interval between arrival of the tracer in the aortic root and the onset of its extraction in different myocardial areas. - Patients with hemodynamically significant coronary artery stenoses (greater than or equal to 75%) revealed a significant increase in coronary transit times over septum, apex, or posterolateral wall of the left ventricle. Using maximal coronary transit times, i.e., the largest of the regional values, an excellent discrimination between patients with severe coronary artery stenoses and controls was achieved. Following coronary vasodilatation with dipyridamole, even subcritical (50-75%) coronary artery stenoses could be detected with high sensitivity, since the shortening of coronary transit times in patients with subcritical stenoses was less pronounced as compared to controls. - Especially in the presence of diffuse three-vessel coronary artery disease, the quantitative assessment of regional coronary transit times yields important parametric data in addition to those obtained by conventional Thallium-201 scintigraphy combining static imaging with rapid sequence analysis of time-activity curves.

Daß Vaskulitiden entsprechend ihrem Charakter als Systemerkrankungen durch Beteiligung der Koronararterien zu einer koronaren Herzerkrankung (KHK) führen können, ist unseres Erachtens zu wenig bekannt. Die Autoren beobachteten innerhalb 1 Jahres vier Fälle, die die angebliche Seltenheit der Koronariitis überdenken lassen.

Hemodynamic function and overall coronary blood flow (argon technique) were measured in 16 patients with idiopathic dilated cardiomyopathy (IDC) and in 12 patients without detectable heart disease (control subjects) referred for precordial pain. In patients with IDC, coronary blood flow was normal at rest (78 +/- 17 ml/100 g-min versus 78 +/- 9 in control subjects). During maximal inducible coronary vasodilation (dipyridamole, 0.5 mg/kg), coronary blood flow was significantly reduced (142 +/- 38 ml/100 g.min versus 301 +/- 64 in control subjects; p less than 0.001). Consequently, obtainable minimal coronary resistance was increased in IDC (0.54 +/- 0.20 mm Hg/ml/100 g.min versus 0.23 +/- 0.04 in control subjects; p less than 0.001). In patients with IDC, left ventricular (LV) end-diastolic pressure was significantly increased (19 +/- 11 mm Hg versus 6 +/- 3 in control subjects; p less than 0.005), and the LV ejection fraction was diminished (36 +/- 11% versus 72 +/- 3% in control subjects; p less than 0.001). In patients with IDC, LV end-diastolic pressure correlated significantly with the obtained minimal coronary resistance after application of dipyridamole (r = 0.85; p less than 0.001). LV catheter biopsy specimens revealed no alterations in myocardial microvasculature. Thus, coronary dilatory capacity is impaired in patients with IDC, due partially to an increase in extravascular component of coronary resistance.

The etiology of congestive cardiomyopathy remains unknown in most patients. Special interest has therefore been paid to the pathophysiological aspects of this disease, because possible relations with the pathogenesis and the natural history may be illuminated. Three main topics will be discussed in detail:

The effects of short episodes (1 min) of vagally-mediated bradycardia were studied in 9 anesthetized dogs utilizing vagal stimulation and slow atrial pacing (120 and 80 beats/min) before and after graded coronary constriction of the left anterior descending (LAD) and the left circumflex (CCA). In the presence of 90% LAD stenosis, bradycardia tended to restore both the elevated total LAD coronary vascular resistance (CVR-LAD) and the reduced, total CVR-CCA towards control levels obtained at corresponding slow rates in the absence of coronary stenosis; as a result, LAD coronary flow (F-LAD) was relatively less reduced and the accessory rise of F-CCA disappeared. In the presence of combination of 90% LAD plus 70% CCA stenosis, the effects of bradycardia on total CVR-LAD and F-LAD were similar to those obtained with single 90% LAD stenosis, but the accessory flow through the CCA was abolished resulting in no significant difference of the rate-dependent alterations of total CVR-CCA and F-CCA as compared with those observed in the absence of coronary stenosis. In the presence of single or combined coronary stenosis, bradycardia restored the depressed aortic pressure and cardiac output towards control values obtained at comparable slow rates before coronary stenosis. The results support the concept that in the presence of 90% LAD stenosis vagally-mediated bradycardia 1) decreases the tension-time index (myocardial nutritional demand) shifting cardiac performance to less expensive "flow work" and 2) facilitates antegrade flow through the highly stenotic LAD thereby inhibiting accessory flow through the nonstenotic CCA.

Forty-eight patients with symptoms of angina pectoris were studied for adipose tissue fatty acid composition and cardiovascular risk factors while hospitalized for selective coronary angiography. Patients with manifest diabetes mellitus and deviations from the “normal” customary diet were excluded.