Arterial stiffness in acute COVID-19 and potential associations with clinical outcome.

BACKGROUND: Coronavirus disease 2019 (COVID-19) interferes with the vascular endothelium. It is not known whether COVID-19 additionally affects arterial stiffness. METHODS: This case-control study compared brachial-ankle pulse wave (baPWV) and carotid-femoral pulse wave velocities (cfPWV) of acutely ill patients with and without COVID-19. RESULTS: Twenty-two COVID-19 patients (50% females, 77 [67-84] years) were compared with 22 age- and sex-matched controls. In COVID-19 patients, baPWV (19.9 [18.4-21.0] vs. 16.0 [14.2-20.4], P = 0.02) and cfPWV (14.3 [13.4-16.0] vs. 11.0 [9.5-14.6], P = 0.01) were higher than in the controls. In multiple regression analysis, COVID-19 was independently associated with higher cfPWV (ß = 3.164, P = 0.004) and baPWV (ß = 3.532, P = 0.003). PWV values were higher in nonsurvivors. In survivors, PWV correlated with length of hospital stay. CONCLUSION: COVID-19 appears to be related to an enhanced PWV reflecting an increase in arterial stiffness. Higher PWV might be related to an increased length of hospital stay and mortality.

"Overestimation" of catheter gradients by Doppler ultrasound in patients with aortic stenosis: a predictable manifestation of pressure recovery.

OBJECTIVES: This study sought to evaluate whether pressure recovery can cause significant differences between Doppler and catheter gradients in patients with aortic stenosis, and whether these differences can be predicted by Doppler echocardiography. BACKGROUND: Pressure recovery has been shown to be a source of discrepancy between Doppler and catheter gradients across aortic stenoses in vitro. However, the clinical relevance of this phenomenon for the Doppler assessment of aortic stenosis has not been evaluated in patients. METHODS: Twenty-three patients with various degrees of aortic stenosis were studied with Doppler echocardiography and catheter technique within 24 h. Using an equation previously validated in vitro, pressure recovery was estimated from peak transvalvular velocity, aortic valve area and cross-sectional area of the ascending aorta and compared with the observed differences between Doppler and catheter gradients. Doppler gradients were also corrected by subtracting the predicted pressure recovery and then were compared with the observed catheter gradients. RESULTS: Predicted differences between Doppler and catheter gradients due to pressure recovery ranged from 5 to 82 mm Hg (mean +/- SD, 19 +/- 16 mm Hg) and 3 to 54 mm Hg (12 +/- 11 mm Hg) for peak and mean gradients, respectively. They compared well with the observed Doppler-catheter gradient differences, ranging from -5 to 75 mm Hg (18 +/- 18 mm Hg) and -7 to 48 mm Hg (11 +/- 13 mm Hg). Good correlation between predicted pressure recovery and observed gradient differences was found (r = 0.90 and 0.85, respectively). Both the noncorrected and the corrected Doppler gradients correlated well with the catheter gradients (r = 0.93-0.97). However, noncorrected Doppler gradients significantly overestimated the catheter gradients (slopes, 1.36 and 1.25 for peak and mean gradients, respectively), while Doppler gradients corrected for pressure recovery showed good agreement with catheter gradients (slopes, 1.03 and 0.96; standard error of estimate [SEE] 8.1 and 6.9 mm Hg; mean difference +/- SD 0.4 +/- 8.0 mm Hg and 1.1 +/- 6.8 mm Hg for peak and mean gradients, respectively). CONCLUSIONS: Significant pressure recovery can occur in patients with aortic stenosis and can cause discrepancies between Doppler and catheter gradients. However, pressure recovery and the resulting differences between Doppler and catheter measurements may be predicted from Doppler velocity, aortic valve area and size of the ascending aorta.

Impairment of endothelium-independent vasodilation in patients with hypercalcemia.

OBJECTIVE: Patients with primary hyperparathyroidism (PHPT) and/or hypercalcemia are at increased risk for myocardial ischemia. Whether PHPT is associated with altered endothelium-dependent dilation, vascular smooth muscle cell function, or both is unknown. This study was performed to test the hypothesis that endothelium-dependent, flow-mediated dilation (FMD) and/or endothelium-independent, nitroglycerin-induced dilation (NMD) is impaired in the preclinical phase of vascular disease in patients with PHPT. METHODS: Twenty-six PHPT patients (mean +/- SD; age 55 +/- 15 y, serum calcium 3.00 +/- 0.37 mmol/l, serum phosphate 0.79 +/- 0.21 mmol/l, iPTH 249 +/- 262 pg/ml) with no evidence of coronary artery disease (CAD) as well as 26 normocalcemic control subjects (CTL; age 51 +/- 12 y) were studied. FMD following reactive hyperemia and NMD after 0.8 mg nitroglycerin (NTG) were assessed in the brachial artery by using high resolution ultrasound (7 MHz). RESULTS: NMD was impaired in PHPT patients compared to CTL (11.9 +/- 3.9% vs. 15.6 +/- 5.7%; p = 0.012). FMD was similar in both study groups (11.6 +/- 4.6% vs. 12.6 +/- 4.9; NS). The ratio of FMD to NMD was significantly different between PHPT patients and CTL (0.98 +/- 0.19 vs 0.81 +/- 0.25, p = 0.0009). On multiple stepwise regression analysis serum calcium was independently associated with the FMD/NMD ratio (r = 0.34, p = 0.017). CONCLUSIONS: Endothelium-independent vasodilation is impaired in PHPT patients without clinical evidence of coronary artery disease compared to normocalcemic CTL, while endothelium-dependent dilation was similar in both study groups. Thus, altered arterial reactivity in the course of PHPT may predominantly involve the arterial media and not the endothelium as observed previously in patients with various stages of atherosclerosis.

Accumulation of oxidized LDL in human semilunar valves correlates with coronary atherosclerosis.

OBJECTIVE: Recent data indicate that oxidized low-density lipoprotein (ox-LDL) has several proatherogenic effects, e.g. induction of macrophage chemoattractants, adhesion molecules, cytokines, type-1 plasminogen activator inhibitor and platelet-derived growth factor A-chain by smooth muscle cells. Therefore, ox-LDL has been utilized as a marker of oxidative modification of proteins in atherosclerosis. Because heart valves consist of smooth muscle cells, fibroblasts and endothelial cells, and because valvular disease and coronary atherosclerosis could result from similar biological processes, we investigated ox-LDL accumulation in isolated aortic and pulmonary valves and coronary arteries from patients with angiographically proven coronary heart disease (CHD, n = 19), patients with idiopathic congestive heart failure (IDCM = idiopathic dilated cardiomyopathy, n = 20), and transplant donors. METHODS: Masson-Goldner staining and immunohistochemistry utilizing anti ox-LDL and CD68 were performed on paraffin sections of freshly isolated semilunar valves. Data were analyzed by digital image planimetry and by visual scoring of staining intensity. RESULTS: Ox-LDL immunoreactivity was identified in the vascular aspect of the attachment line, in the deep valve stroma, and in the ventricular and vascular endothelium of the semilunar valves, colocalizing with macrophages. Valvular ox-LDL area was significantly increased in CHD-patients (P < 0.03) and IDCM-patients (P < 0.04) compared with controls. More ox-LDL was accumulating in the pulmonary valves than in the aortic valves (P = 0.04) as assessed by area and staining intensity. Valvular ox-LDL area in pulmonary valve and aortic valve was significantly correlated with ox-LDL accumulation in the intimal layer (P < 0.001) and medial layer (P < 0.001) of coronary arteries from the same patients. CONCLUSION: The data suggest that the biological process leading to ox-LDL accumulation in coronary atherosclerosis also involves heart valves. Therefore, accumulation of the oxidative stress marker ox-LDL in heart valves illustrates atherosclerosis as an additional mechanisms accelerating valvular degeneration in these patients.

Cardiac abnormalities in patients with primary hyperparathyroidism: implications for follow-up.

Patients with primary hyperparathyroidism (PHPT) show a high incidence of left ventricular hypertrophy, cardiac calcific deposits in the myocardium, and/or aortic and mitral valve calcification and thus may carry an increased risk of death from circulatory diseases. This prospective study was designed to assess an effect of parathyroidectomy on cardiac abnormalities of patients with PHPT. Echocardiography was used to evaluate the mechanical performance of the heart muscle, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications within 12 and 41 months after parathyroidectomy. In a blinded fashion, aortic and mitral value calcifications were determined in 46% and 39% of patients with PHPT. Calcific deposits in the myocardium were found in 74% of patients. Follow-up studies after parathyroidectomy disclosed no evidence of progression of these calcifications. Before operation left ventricular hypertrophy was detected in 82%. After parathyroidectomy and 41 months of normocalcemia and normal PTH concentrations, a regression of hypertrophy of the interventricular septum and the posterior wall by -6% and -19% (P < 0.05) was observed. Subgroup analysis disclosed the most impressive long-term reduction of left ventricular hypertrophy in patients without a history of hypertension (-11% and -21%; P < 0.05 and P < 0.005); no changes were determined in 9 patients who developed secondary hyperparathyroidism after operation. The present data show a high incidence of left ventricular hypertrophy and aortic and/or mitral valve calcifications in patients with PHPT. Follow-up at 1 year and at 41 months after successful parathyroidectomy disclose regression of hypertrophy. Our results give evidence that parathyroid hormone per se plays an important role in the maintainance of myocardial hypertrophy. Post-surgical restoration of normocalcemia and normalization of parathyroid hormone valvular sclerosis persists without evidence of progression. We further conclude that patients with PHPT and parathyroidectomy are at low risk for the development of severe aortic and mitral valve stenosis within this period of time.

Urinary apo(a) discriminates coronary artery disease patients from controls.

Increased plasma lipoprotein (a) (Lp(a)) levels are associated with premature cardiovascular diseases and stroke. Since Lp(a) immune reactivity is found in urine we compared urinary apolipoprotein (a) (apo(a)) with plasma Lp(a) levels in 116 patients suffering from angiographically proven coronary artery diseases with that of 109 controls. Urinary apo(a) investigated by immuno blotting, revealed a distinct apo(a) fragmentation pattern with molecular weights between 50 and 160 kDa. Apolipoprotein B however was not secreted into urine. Lp(a) and apo(a) were measured by a fluorescence immuno assay. Within single individuals, urinary apo(a) levels correlated significantly with creatinine (Rho, 0.98; P < 0.0005). Medians and 25/75 percentiles of urinary apo(a) in coronary artery disease (CAD) patients were 5.70, 3.25 and 10.35 microg/dl and in controls 2.64, 1.43 and 3.50 microg/dl respectively. At cut-off levels of 30 mg/dl for plasma Lp(a) and 10 microg/dl of urinary apo(a) respectively, both paramenters showed comparable sensitivities (33.8% vs. 26.7%), yet the specificity (76.1% vs. 91.7%) and the positive predictive value (60.0% vs.76.4%) of urinary apo(a) were much higher. In receiver-operating characteristic plots, urinary apo(a) was much more sensitive at high specificities i.e. greater than 60% as compared to Lp(a). Urinary secretion of apo(a) fragments normalized to creatinine is stable in a given individual and significantly associated with coronary artery disease.

Primary hyperparathyroidism: incidence of cardiac abnormalities and partial reversibility after successful parathyroidectomy.

PURPOSE: This prospective study was designed to assess the effect of primary hyperparathyroidism on heart muscle, valves, and myocardial function. Echocardiography was used to evaluate changes in mechanical performance, the thickness of the left ventricular wall, myocardial calcific deposits, and valvular calcifications in patients with primary hyperparathyroidism. METHODS: Echocardiography was performed in 54 patients with hyperparathyroidism prior to surgery and 12 +/- 2 months after successful parathyroidectomy. A matched control group was followed for comparison. RESULTS: In a blinded fashion, aortic and mitral valve calcifications were detected in 63% and 49% of patients with primary hyperparathyroidism (controls: 12% and 15%, respectively). Calcific deposits in the myocardium were found in 69% of patients with hyperparathyroidism and 17% of the control subjects. After parathyroidectomy and 12 months of normocalcemia, a significant regression of left ventricular hypertrophy (p < 0.001) was observed. CONCLUSIONS: The present data show a high incidence of left ventricular hypertrophy, calcific deposits in the myocardium, and/or aortic and mitral valve calcification in patients with primary hyperparathyroidism. A 1-year follow-up after parathyroidectomy (and restoration of normocalcemia) discloses regression of hypertrophy, while calcifications persist without evidence of progression.

Plasminogen activator inhibitor-1 levels in patients with chronic angina pectoris with or without angiographic evidence of coronary sclerosis.

Increased plasma levels of plasminogen activator inhibitor-1 (PAI-1) have been shown to exist in 40 to 60% of patients with stable coronary artery disease and have been suggested to be responsible for the development of coronary thrombotic complications. However, it is also discussed whether PAI-1 elevation might mainly be due to variables like increased age or to reactive mechanisms caused e.g. by the chest pain itself. To exclude age dependent or pain related influences, age-matched patients with stable angina pectoris (NHYA II) and angiographically proven coronary artery disease (CAD, n = 16) or without evidence for coronary sclerosis (variant angina, n = 10; angina-like syndrome with normal coronary angiogram, n = 5; non-CAD, n = 15) have been investigated for their plasma PAI-1 activity and t-PA antigen levels. The mean PAI activity in CAD patients (17.5 U/ml) was significantly higher than in non-CAD patients (9.6 U/ml) (p less than 0.0001). In the CAD patients no significant variation in plasma PAI-1 values could be demonstrated when related to the extent of the disease or to a history of previous myocardial infarction. t-PA antigen was also elevated in CAD patients as compared to the non-CAD group (p less than 0.02). The results suggest therefore a strong correlation between coronary artery disease itself and elevated levels of components of the plasma fibrinolytic system.

Implantable cardioverter-defibrillator dysfunction after coronary artery bypass grafting.

Displacement of an ICD electrode is a possible complication after changes in heart size after CABG and simultaneous implantation of an epicardial lead ICD. To prevent potentially life-threatening ICD dysfunction in patients who are candidates for CABG and ICD implantation, we suggest the use of transvenous ICD systems or a staged procedure (CABG followed by ICD implantation) rather than a simultaneous operation.

Informational contribution of noninvasive screening tests for coronary artery disease in patients on chronic renal replacement therapy.

The prevalence of coronary artery disease (CAD) is high in patients on renal replacement therapy; therefore, reliable noninvasive screening tests are needed. We retrospectively determined the sensitivity, specificity, and positive and negative likelihood ratios (LRs) for a history of chest pain, resting and exercise electrocardiography (ECG), thallium dipyridamole scintigraphy, and echocardiography in 42 patients undergoing chronic hemodialysis and 42 patients after renal transplantation who also underwent coronary angiography. In addition, the prognostic power of each test for the occurrence of a cardiovascular event after angiography (therapeutic intervention, myocardial infarction, or cardiovascular death) was evaluated during a follow-up of 37 months. Forty-three patients had significant CAD on angiography. Angina pectoris had a sensitivity of 65% and specificity of 66%, corresponding to a positive LR of 1.9 and a negative LR of 0.5. A variable number of patients underwent noninvasive tests before angiography. Results were similar in patients undergoing hemodialysis and after renal transplantation and in patients with or without angina pectoris. Exercise ECG could not be performed in the majority of patients, and resting ECG (sensitivity, 67%; specificity, 52%; corresponding to a positive LR of 1.4 and negative LR of 0.6) and scintigraphy (sensitivity, 80%; specificity, 37%; positive LR, 1.3; negative LR, 0.5) in patients on renal replacement therapy were not useful for the diagnosis of CAD. Angina also markedly increased the relative odds for the occurrence of a cardiovascular event during follow-up (relative odds, 4.6) compared with other noninvasive tests. Angina pectoris had the best informational and prognostic value of noninvasive screening methods, but angiography seems to be the only method to clearly document CAD in patients on renal replacement therapy.

Response of right ventricular function to prostaglandin E1 infusion predicts outcome for severe chronic heart failure patients awaiting urgent transplantation.

BACKGROUND: Selection of patients for urgent heart transplantation who have end-stage heart failure requires objective criteria to distinguish between subjects who may deteriorate clinically and those who can be stabilized. This population appears to differ in terms of right ventricular function, and right ventricular changes in loading may provide prognostic information. To investigate predictive parameters of patients admitted for urgent heart transplantation, we prospectively studied the mechanical performance of the right ventricle during acute afterload reduction. PATIENTS AND METHODS: We studied 68 heart failure patients hospitalized for bridge-to-transplant. The patients underwent right heart catherization at baseline and during prostaglandin E1 infusion. We stratified patients according to clinical outcome: Group A comprised patients who could be weaned from bridging therapy or who were electively transplanted after at least 90 days, and Group B comprised patients who died or who remained unstable and required transplant under urgent conditions. RESULTS: Right ventricular hemodynamics at baseline were comparable in both groups. However, during maximal vasodilatation, with prostaglandin E1 infusion, the right ventricular end-diastolic volume index (EDVI) was significantly reduced in Group A, (-23 ml/m(2) (p < 0.01) vs +12 ml/m(2) (p = n.s. DeltaEDVI in Group B. Reduction of EDVI by less than 10% during prostaglandin E1 infusion has a sensitivity of 89% and a specificity of 70% for clinical deterioration. CONCLUSIONS: The response of right ventricular volumes to prostaglandin E1 may predict the outcome of patients with severe congestive heart failure listed for urgent heart transplantation.

Time course of regression of left ventricular hypertrophy after successful parathyroidectomy.

BACKGROUND: We have shown that primary hyperparathyroidism may induce myocardial hypertrophy that is reversible after successful parathyroidectomy. The present study was designed to assess the time course of regression of left ventricular hypertrophy without further effects of drug treatment or disease states. METHODS: We performed echocardiographic studies in 16 patients with primary hyperparathyroidism and normal resting blood pressure, normal systolic left ventricular function, no evidence of valvular disease, and without any current medication before parathyroidectomy, as well as during intermediate and long-term follow-up after successful parathyroidectomy. RESULTS: Eleven patients (69%) had end-diastolic wall thickness of the interventicular septum and/or posterior wall greater than 11 mm on baseline echocardiogram. After surgical removal of the inciting disease and an average of 12.5 and 45.7 months of follow-up with normocalcemia and normal parathyroid hormone levels a prolonged regression of left ventricular hypertrophy was observed (interventricular septum, -0.68 mm at 12.5 months and -1.69 mm at 45.7 months; p = 0.02; posterior wall, -0.46 mm at 12.5 months and -2.24 mm at 45.7 months; p = 0.02). CONCLUSIONS: We conclude that the removal of the cause of myocardial hypertrophy by successful parathyroidectomy leads to a prolonged reversal of hypertrophy. The progressive reduction of left ventricular wall thickness is not completed within 12 months.

Cardiac calcific deposits in patients with primary hyperparathyroidism: preliminary results of a prospective echocardiographic study.

To explain the incidence and significance of mitral and aortic valve calcification and calcific deposits in the myocardium, a prospective echocardiographic study was performed with 21 consecutive patients who had primary hyperparathyroidism (PHP) and with 21 age- and sex-matched control subjects with normocalcemia. Calcific deposits in the myocardium were seen in 13 patients (62%) with PHP, mainly in the interventicular septum, and in one control subject. Aortic valve calcification was observed in 12 patients (57%) with PHP and in one control subject. Calcification of the mitral valve was found in seven patients with PHP (33%) and three controls (14%). Calcification led to mild or moderate stenosis of the aortic valve in three patients with PHP and of the mitral valve in two patients with PHP. No stenosis was found in the subjects in the control group. Both calcification of the aortic and mitral valves and calcific deposits in the myocardium are common in patients with PHP and can be detected noninvasively by echocardiography. Because of the potential relationship of elevated calcium, calcification, and valvular heart disease, clinical evaluation of PHP should include echocardiographic studies before surgery is performed and during follow-up examination.

In vitro evaluation of the anticancer drug modulatory effect of hyaluronidase in human gastrointestinal cell lines.

In an attempt to establish whether the combination of anticancer drugs with hyaluronidase would result in enhanced cytotoxicity, we have tested a range of 6 continuous cell lines against 4 different chemotherapeutic drugs with or without the addition of various concentrations of the enzyme. Measurement of cytotoxic drug effects has been performed using the Bactec system, a new semiautomated radiometric technique. In only 15 of a total of 144 experiments (11%) was a significant hyaluronidase-mediated potentiation of the single agents' activity seen. In the large majority of experiments, the antiproliferative effect of the combined treatment was classified as additive or subadditive, while in 23% it was antagonistic. Evaluation of the drug modulatory mechanism of hyaluronidase suggested that the combined drug-hyaluronidase effects were independent of the nature of the drug, the exposure mode and the concentration of the enzyme employed. Among the various tumor cell lines tested there was a marked heterogeneity in the sensitivity to the combined effect (P less than 0.0001). In summary, we have not been able to confirm the promising results of early reports of in vitro and in vivo enhancement of the cytotoxicity of antitumor agents by hyaluronidase. Our data emphasize the need for further controlled clinical studies in order to prove or disprove this new therapeutic approach.

Increase of pulmonary vascular resistance during cold provocation in patients with variant angina.

This study was performed to evaluate pulmonary vascular reactivity in patients with angiographically documented coronary vasospasm. Right heart catheterization was performed in 8 subjects with vasospastic angina without evidence of Raynaud's phenomenon: heart rate, systemic and pulmonary arterial pressure as well as cardiac output were determined at rest, during cold provocation and after 20 minutes recovery. Data were obtained both before and during treatment with nifedipine. During cold provocation pulmonary vascular resistance was elevated significantly (P less than 0.02 compared with baseline); systemic vascular resistance tended to increase; nifedipine blunted both vasoconstrictor effects. Our results indicate an abnormal vascular response of the pulmonary arteries to cold provocation in patients with symptomatic coronary artery spasm and suggest a primary vasospastic disorder with coronary and pulmonary manifestation.

Humoral regulation during cold-induced coronary arterial spasm.

Previous attempts to define the etiology of coronary arterial spasm have been focused on mechanisms such as autonomic nervous dysfunction and/or enhanced platelet activation. In the present study, humoral regulation was investigated in patients with vasospastic angina and scintigraphically documented transient myocardial perfusion abnormalities after a peripheral cold pressor test. Serial changes in angiotensin II, epi- and norepinephrine as well as thromboxane B2 (the stable derivate of thromboxane A2), and malondialdehyde were determined at baseline (I), immediately after 5 minutes cold water hand immersion (II), and following 10 minutes recovery (III). Angiotensin II and epinephrine remained unchanged during observation (I vs II, II vs III: P = NS). Norepinephrine was elevated after cold (I vs II: P less than 0.001) and normalized after 10 minutes (I vs III: P = ns). Thromboxane B2 and malondialdehyde increased continuously (I vs III: P less than 0.05 and I vs III: P less than 0.002, respectively). Further radiothin-layer chromatography results indicate an activation of platelet function during myocardial ischemia. Our results do not establish a cause-effect relationship but, together with other evidence, they may suggest that thromboxane A2 is unlikely to be the cause of spasm. It might, however, play an important role in the maintenance of vasoconstriction.

Cardial decompensation caused by hypertension and polyglobulia associated with multiple renal oncocytomas.

A 43 year old man was referred to the Internal Department for the examination of cardial decompensation, hypertension, polyglobulia and atrophy blanche of the lower legs. Clinical and supersonic examination revealed two tumors in the left kidney (diameter 8 and 3.5 cm) and some small tumors in the right kidney. Laboratory studies disclosed erythropoietin levels up to 170 mU/ml (standard 14-61 mU/ml) and a red blood cell count of up to 8 X 10(6)/ml. After recompensation, a radical left nephrectomy and the removal of three small tumors of the right kidney four weeks later was initiated. Postoperative erythropoietin levels and red blood cell count sank to the normal range leading to the reduction of antihypertensive therapy. The clinical course indicates a strong etiological connection between hypertension as well as polyglobulia with the multiple bilateral oncocytomas. Polycythemia also led to the atrophy blanche which had resulted from disturbances of microcirculation.

[Importance of intracellular calcium homeostasis for contraction and relaxation of the heart muscle]. / Die Bedeutung der intrazellulären Kalziumhomöostase für die Kontraktion und Relaxation des Herzmuskels.

The method of surface fluorometry with indo-1 allows the simultaneous quantitative recording of changes in free intracellular calcium ([Ca2+]i) transients during the cardiac cycle and haemodynamic parameters and ECG. Using this method, recent studies gave further insight into acute and chronic changes in [Ca2+]i during disease (e.g. heart failure, ischaemia, arrhythmias), as well as pharmacologic interventions. The failing myocyte is characterized by small calcium transients and elevated end-diastolic [Ca2+]i concentrations. Without an adequate delivery of substrate to the mitochondria (pyruvate, but not glucose) the cardiomyopathic heart muscle is no longer capable of maintaining its [Ca2+]i homeostasis. In healthy hearts, positive inotropic agents lead to an increase in developed pressure commensurately with the percentage changes in amplitude of the [Ca2+]i transients, while the end-diastolic [Ca2+]i levels seem to depend on the activation of cAMP. In failing hearts the latter finding may explain the different behaviour of end-diastolic [Ca2+]i and haemodynamics during perfusion with various catecholamines, more likely stimulating alpha- and/or beta-adrenoceptors. Further studies analysed [Ca2+]i during ischaemia or showed the importance of changes of [Ca2+]i in the genesis of premature beats and the initiation of tachyarrhythmias, in particular ventricular fibrillation. The present overview underlines the comprehensive role of calcium homeostasis in the pathophysiology of contraction and relaxation of the heart muscle.

[Myelosarcoma of the ovary]. / Myelosarkom des Ovars.

The case is reported of a patient with granulocytic sarcoma of the right ovary and infiltration of granulocytic precursor cells into abdominal lymph nodes without any evidence of acute leukaemia on examination of the blood and bone marrow. Removal of the tumour and subsequent polychemotherapy was followed by remission. A local recurrence was treated with radiation and high-dose polychemotherapy. The patient has now been in complete remission for seven years. Thus, granulocytic sarcoma may have a good prognosis if treated with aggressive therapy, including operation, radiation, and high-dosage polychemotherapy.

Emergency angioplasty and stent deployment for acute occlusion of an anomalous single coronary artery (all three coronary arteries from one ostium in the right sinus of Valsalva).

A single coronary ostium is traditionally considered to be of little clinical significance. We report a case of a single ostium in the right sinus of Valsalva, giving rise to the right coronary artery, from which the left main coronary artery originated. Sudden death occurred seven days after acute gastrointestinal bleeding and subsequent interruption of aspirin therapy. Acute coronary angiography following successful resuscitation revealed an ascending thrombus in the right coronary artery. The patient underwent a complex percutaneous coronary angioplasty with stent deployment. We conclude that coronary artery disease may lead to severe ischemia with a large area at risk and major complications in patients with coronary anomalies. Patients with acute stent implantation might benefit from platelet aggregation even in cases of recent intestinal bleeding.