Segmental degradation of left ventricular wall motion after persistent coronary fistula in a posttransplantation patient: a case report and short review of literature.

A 50-year-old man received an orthotopic heart transplant because of severe coronary heart disease and congestive heart failure. Two years after the transplantation, a continuous murmur occurred at the left sternal edge after repeated endomyocardial biopsies. Echocardiography and coronary angiography revealed a dilated left anterior descending artery with a fistula to the right ventricle. The circumflex was large with an equally postero-lateral branch, and the right coronary artery was rather small with collaterals to the distal part of the left anterior descending branch. The patient had refused any intervention to close the fistula. The left ventricular levogram was normal. Two years later, in a follow-up angiogram, the left ventricular ejection fraction had decreased as a result of hypo- and akinesis of the apex and posterior wall. We suggest that this local wall motion disturbance derives from a steal phenomenon rather than being a sequela of rejection. The decrease in left ventricular ejection fraction was associated with shortness of breath upon moderate exercise. Standard heart failure medication relieved the patient's symptoms. The observation of local wall motion disturbances in this case, as well as conflicting views in the literature, raises the question whether postbiopsy coronary fistulas in transplant patients should be closed.

EDRF does not mediate coronary vasodilation secondary to simulated ischemia: a study on KATP channels and N omega-nitro-L-arginine on coronary perfusion pressure in isolated Langendorff-perfused guinea-pig hearts.

Several authors have alluded to the possible involvement of EDRF (NO) in ischemia-induced coronary artery dilation. Alternatively, it has been suggested that opening of ATP-dependent K channels could play a key role in this context. We studied the effects of sulfonylureas and NG-nitro-L-arginine (LNNA), a specific inhibitor of endothelial NO (EDRF) synthesis, on ischemia-induced coronary vasodilation in isolated Langendorff-perfused guinea pig hearts arrested with 15 mM KCl in normal Tyrode, and isolated pig coronary arteries precontracted with 43 mM KCl. In Isolated Langerdorff-perfused guinea pig heart, when hypoxia was simulated by switching 100% O2 in the perfusate to 100% N2, coronary perfusion pressure (CPP) fell from 90 cm H2O by 45 +/- 5 cm H2O. In the presence of LNNA, a specific inhibitor of NO synthetase in endothelial cells, CPP dropped by 44 +/- 6 cm H2O (n = 6; +/- SEM, no statistically significant). On biochemical simulation of ischemia (addition of iodoacetate [IAA]), CPP dropped 40 +/- 6 cm H2O, and in experiments performed under the same conditions but in the presence of LNNA, CPP dropped by 38 +/- 5 cm H2O (n = 6; +/- SEM; not statistically significant). When ischemia was simulated metabolically by equimolar replacement of 10 mM glucose with 2-deoxyglucose (DOG), an inhibitor of glycolysis CPP decreased by 24 +/- 1 cm H2O (n = 6; +/- SEM) after 15 minutes. This fall in CPP was almost prevented by 20 microM glibenclamide, whereas in the presence of 20 microM LNNA the DOG-induced decrease in CPP was not significantly inhibited, and CPP decreased by 22 +/- 2.6 cm H2O (n = 6; +/- SEM). In isolated pig coronary artery rings, maximal tension, achieved by depolarizing the smooth muscle cells by 43 mM KCl, decreased by 37 +/- 7% upon simulated hypoxia by replacing 100% O2 with 100% N2 in the perfusate (n = 6; +/- SEM) in arteries with intact endothelium. In arteries without endothelium, maximal tension also dropped by 35 +/- 6% (not statistically significant). In the same experiments the decrease in tension could be largely inhibited in the presence of 50 microM glibenclamide. Our results clearly show that in isolated perfused guinea pig hearts, as well as in isolated pig coronary arteries, EDRF does not play a decisive role in the coronary dilatory response to hypoxia and ischemia.

Near fatal anticholinergic intoxication after routine fundoscopy.

We describe a case of severe anticholinergic intoxication following the topical instillation of tropicamide-containing eyedrops. Tropicamide is a short-acting atropine-like derivative and has been regarded as an effective and safe mydriatic. Half an hour after routine fundoscopy, a 62-year-old man experienced two generalized seizures with respiratory arrest and required intubation and mechanical ventilation. The patient was treated with physostigmine and made a full recovery.

[Physical activity at intermediate altitude by healthy probands and patients with coronary sclerosis]. / Körperliche Aktivität in mittleren Höhenlagen bei Gesunden und Patienten mit Koronarsklerose.

For the majority of the population, exposure to altitudes higher than 2000 m above sea level constitutes a situation of pronounced stimulation of the organism. The question comes in of the health relevance of physical activity at intermediate altitudes for the healthy subjects, but above all for people with heart problems. At first, there is an acute adaption on the cardiovascular and the respiration system as well as the system of oxygen carriage, until the chronic adaption processes of the same systems are completed. Doubtlessly, these adaption processes at intermediate altitudes and in particular training in such regions considerably improve the endurance capacity under conditions of the kind mentioned. However there is little evidence, for an absolute improvement of the maximal aerobic capacity. As a rule, the effects of adaption to higher altitudes can also be expected in patients with coronary sclerosis. But a lowered level of capacity must be taken into account in these cases. Accordingly, the medication as well as the intensity of stress should be adapted to altered conditions of this kind. Training intensity must be reduced according to altitude, and any treatment for angina, must be intensified. It may be necessary to re-determine the appropriate training intensity as well as the dosage in pharmacotherapy by ergometric methods to match the new requirements. However, when a comparison is tried to kinetotherapy under normal conditions, an immediate therapeutical effect of exposition to higher altitudes appears to be at least doubtful.

Increased red cell 2,3-diphosphoglycerate levels in haemodialysis patients treated with erythropoietin.

The efficacy of recombinant human erythropoietin (rHuEpo) for the treatment of renal anaemia is well established. To assess the effect of rHuEpo treatment on physical performance we evaluated physical working capacity, oxygen uptake and red cell 2,3-diphosphoglycerate (DPG) values at rest and during and after exercise on a bicycle spiroergometer in eight chronically haemodialysed patients. Follow-up examination was carried out after a mean of 14 weeks (range 9-19 weeks), when mean haemoglobin had increased from 7.8 to a stable value of 13.0 g/dl in response to rHuEpo treatment (P < 0.001). Physical working capacity and oxygen uptake at the anaerobic threshold (4 mmol/l blood lactate concentration) increased from 68 +/- 12 to 80 +/- 16 watts and 0.95 +/- 0.14 to 1.10 +/- 0.20 l/min, respectively (P < 0.01). DPG, which determines oxygen affinity to haemoglobin in red cells, increased by 13% from 13.7 +/- 1.5 to 15.5 +/- 2.2 mumol/g Hb (P < 0.05). With maximal exercise mean DPG values significantly decreased to a much lower level without rHuEpo treatment than after correction of anaemia. Therefore rHuEpo treatment results both in better oxygen transport capacity and reduced intraerythrocytic oxygen affinity, which is followed by improved oxygen delivery to tissues per unit of haemoglobin. These effects may explain the improvement of exercise capacity observed in dialysis patients after rHuEpo treatment.

Evaluation of the antihypertensive effect of lisinopril compared with nifedipine in patients with mild to severe essential hypertension.

For several reasons, increasing numbers of patients with hypertension are treated with angiotensin-converting enzyme inhibitors and calcium channel blockers. In a twenty-four week, double-blind, randomized, parallel study, the antihypertensive effect of lisinopril (20 to 80 mg qd) and nifedipine (20 to 80 mg bid) were compared in 21 patients. Fourteen patients received lisinopril (mean dose 35 mg), and 7 patients received nifedipine (mean dose 54 mg). By the end of week 12, 8 patients had responded (supine diastolic pressure less than or equal to 90 mg) to lisinopril and 5 to nifedipine. At the end of the study supine systolic/diastolic blood pressure was reduced from 172/104 to 149/92 mmHg with lisinopril and from 171/102 to 158/94 mmHg with nifedipine. No significant difference between the two treatments was detected. Three patients were reported to have at least one clinical adverse experience during the active treatment period, 1 in the lisinopril group and 2 in the nifedipine group. No serious clinical adverse experiences were recorded. In conclusion, lisinopril and nifedipine are both effective in reducing blood pressure in patients with mild to severe hypertension. Lisinopril qd and nifedipine slow release bid produce similar decreases in blood pressure after twelve weeks of therapy and the safety profiles of the two drugs are similar.

Frequency of magnetic resonance signal abnormalities of the brain in patients aged less than 50 years with idiopathic dilated cardiomyopathy.

Twenty patients with idiopathic dilated cardiomyopathy (IDC) aged less than 50 years (mean 41) and an age-matched group of 20 healthy volunteers were studied. All subjects were free of cerebrovascular symptoms and risk factors for stroke. Magnetic resonance imaging of the brain, extracranial Doppler ultrasonography, heart catheterization and echocardiography were performed. In patients with IDC, a higher frequency of ventricular enlargement (p less than 0.02), cortical atrophy (p less than 0.01) and white matter lesions (p less than 0.05) was observed. Cerebral infarcts were found in 4 patients (p less than 0.05) who showed clinically severe limitation of functional capacity (New York Heart Association class III or IV). The extent of cortical atrophy, and the duration of clinical evidence of IDC showed a significant correlation (p less than 0.04). The data indicate a high incidence of parenchymal abnormalities of the brain in young, neurologically asymptomatic patients with IDC.

Circadian blood pressure pattern in patients with treated hypertension and left ventricular hypertrophy.

Left ventricular hypertrophy in hypertensives is an important determinant of prognosis. In the present study 45 patients with treated essential hypertension were divided into two groups: 23 patients had normal left ventricular dimension and 22 patients had echocardiographic signs of left ventricular hypertrophy (LVH). All patients were adequately treated during daytime, but ambulatory blood pressure monitoring showed a distinct abnormal pattern in the LVH group characterized by a lack of blood pressure reduction during the night; 16 of 22 patients with LVH had no blood pressure decline during the night, whereas 17 of 23 patients without hypertrophy showed this reduction (P less than 0.01). In conclusion, patients with hypertension and LVH often reveal a lack of blood pressure decline during the night, which may be the reason for the development of left ventricular hypertrophy (and thus should be managed by a different circadian blood pressure therapy) or which may be the consequence of progressive structural changes in the resistance vessels, along with the development of left ventricular hypertrophy. It is suggested that patients with hypertension and left ventricular hypertrophy should have ambulatory twenty-four hour blood pressure monitoring.

New concepts in ischemia prevention.

Transient myocardial ischemia may result from obstruction to flow in the large epicardial coronary arteries or diminished flow reserve due to small vessel disease or left ventricular hypertrophy. In patients with coronary heart disease, calcium blockers have proven to reduce stress induced ischemia in patients with normal left ventricular function and in those with ischemic cardiomyopathy. However, recent studies indicate a need for caution when giving calcium antagonists to patients with postinfarction left ventricular systolic dysfunction. Moreover, calcium antagonists that reduce heart rate (diltiazem) are able as a monotherapy to reduce total ischemic burden. Calcium antagonists that may increase rate (dihydropiridines) have to be combined with beta-blockers to achieve this goal. For 24-h control of ischemia the ischemic threshold should be determined for a differentiated therapy in the individual patient. Is the ischemic threshold of the majority of episodes lower than the exercise threshold, a calcium blocker should work. Angiotensin-converting enzyme (ACE) inhibitors are not effective in stress-induced ischemia, but may reduce total ischemic burden, although this effect is not significant. In patients with left ventricular hypertrophy and/or small vessel disease, calcium blockers and ACE inhibitors are probably effective in regression of left ventricular hypertrophy and vascular hypertrophy. However, it remains to be shown that ischemia is reduced by these drugs.

[Correlation between late potentials, left ventricular function and coronary heart disease]. / Korrelation zwischen Spätpotentialen, Linksventrikulärer Funktion und koronarer Herzkrankheit.

By signal averaging it is possible to registrate late, fragmented low amplitude signals (late potentials, LP's) from the bodysurface 26 patients (21 males, 5 females) with a mean age of 57 years were investigated by signal averaging, Holter-monitoring and cardiac catheterization. 11 patients had a dilative cardiomyopathy (group A), 10 patients a coronary heart disease (group B), 5 of them with an ejection fraction greater than 50%, 5 of them with a reduced ejection fraction, whereas the control-group with 5 patients (group C) showed no coronary stenosis or reduced ventricular function, 6 out of 11 patients with dilative cardiomyopathy showed LP's; all of these with Lown IVb had LP's. In 2 patients with coronary heart disease and good left ventricular function late potentials were found, and in all 5 patients with disturbed left ventricular function. The control-group revealed no late potentials although 4 patients had Lown IVa or more in Holter-ECG. In conclusion, late potentials show a good correlation to malignant ventricular ectopic beats in patients with dilative cardiomyopathy and coronary heart disease, especially when the left ventricular function is reduced.

Anticardiolipin antibodies are no marker for survived myocardial infarction.

Antiphospholipid antibodies--both the lupus anticoagulant and anticardiolipin antibodies--are closely associated with arterial and venous thrombosis. In this prospective trial the IgM- and IgG-anticardiolipin antibodies in serum were determined in acute and chronic coronary artery disease. Seventy-four unselected males (34-87 years, mean 60) were included in the study. All patients underwent coronary angiography; infectious and autoimmune diseases were exclusion criteria. Sixteen patients had coronary artery disease (group A), 34 showed coronary stenoses with prior infarction (B), and 14 had survived an acute myocardial infarction (C), whereas 10 patients revealed no significant coronary narrowing (D; controls). The major risk factors were the same for all groups. Neither the IgM- nor the IgG-anticardiolipin antibody levels showed any significant difference in the four groups. The severity of coronary artery disease did not correlate to these antibodies. Furthermore, no correlation was found between elevated anticardiolipin antibodies and thrombocyte levels. Thus, a higher anticardiolipin level does not appear to be a marker for recurrent cardiovascular events.

[The patient following PTCA]. / Der Patient nach PTCA.

Diagnostic measures after PTCA consist of history, clinical findings, after 3 months and thereafter in 6 months intervals as well as ergometry in case of recurrency of complaints of after 3 months and then in 6 months intervals. A thallium-scintigraphy is done eventually. A repetition of a coronarography is indicated only in cases of typical symptoms or registration of ischemia. Therapy consists of lifelong ASS and calcium channel blockers for 3 months and treatment of risk-factors. Repetition of a PTCA, atherectomy, stent-implantation, laser-angioplasty or bypass-surgery varies from case to case; the decision has to be made individually.