Andreas Lueger

Osteomyelitis of the Spine and Abscess Formation in the Left Thigh after Stent-Graft Implantation in the Superficial Femoral Artery

Purpose: To present a rare case of abscess formation around a covered stent in the superficial femoral artery. Methods and Results: Two weeks after balloon dilation of a left superficial femoral artery (SFA) occlusion, during which a Hemobahn covered stent had been placed to treat dissection, a 77-year-old nondiabetic male developed intolerable pain and swelling of his left thigh. An abscess had formed around the stent, which was patent; intravenous antibiotic therapy quelled the symptoms, and the patient discontinued his oral antibiotic regimen weeks after discharge. General septicemia ensued. Acute lower limb ischemia and excruciating back pain prompted readmission. The SFA stent-graft occlusion required femoropopliteal bypass; the abscess and spondylodiskitis that had developed in the T12 and L1 vertebrae responded to intravenous antibiotics. The patient is without signs of infection at 6 months. Conclusions: Local and systemic infections associated with intraluminal prostheses are rare, and prophylactic antibiotic therapy is not commonly employed. Balloon- or device-induced arterial injury may expose the arterial wall to bacterial colonization, suggesting that patients receiving lengthy stents or experiencing arterial injury during angioplasty should receive antibiotics as a precautionary measure.

The effects of the propranolol enantiomers on the intracardiac electrophysiological activities of Langendorff perfused hearts

SummaryThe optical isomers of the beta blocking agent propranolol exert beta receptor blocking as well as membrane stabilizing effects. The latter is thought to be responsible for the antiarrhythmic effect of the drug.In this study we quantified the electrophysiological effects of both isomers of propranolol on the conduction and pacemaker system of the heart. The experiments were performed on isolated hearts using a special ECG recording and stimulation technique. To abolish isoproterenols beta adrenergic stimulatory effect on heart rate, 30-times higher concentrations of (+)propranolol were necessary than of (−)propranolol in order to be consistent. Both isomers caused a similar and marked slowing of conduction velocity through the bundle of His and ventricular myocardium. Also, heart rate, as well as atrio-ventricular conduction velocity were significantly slowed by a concentration of 10 μM of either drug, (−)propranolol being slightly more effective. Only in the presence of (−)propranolol did significant changes of atrio-ventricular and His-bundle conduction occur at a concentration of 1 μM. During programed stimulation sinus node recovery time was more prolonged by (−)propranolol than during perfusion with (+)propranolol. The highest rate of pacing with 1∶1 conduction of the sino-atrial conduction, the atrial and ventricular myocardium was significantly depressed to a comparable degree by either isomers of propranolol. These effects appear to be primarily responsible for the antiarrhythmic effects of both isomers. Because of the minor effects of (+)propranolol on sinus- and AV-node activity, as well as on beta adrenergic receptors, this isomer may have potential clinical importance in the treatment of arrhythmias.

Aortic dissection due to discontinuation of beta-blocker therapy

beta-Blockers are known to protect a vulnerable aorta from acute dissection, as well as reducing the risk of recurrent dissection. This case presentation reports the history of a 60-year-old male suffering from acute aortic dissection following discontinuation of beta-blocker therapy. The patient has shown arterial hypertension for about 20 years treated solely by beta-blockers. Two days after stopping the use of metoprolol, a nonselective beta 1-blocker without ISA, the patient developed severe chest pain during exercise. Diagnosis of type I-aortic dissection according to DeBakey was achieved by transthoracal echocardiography and computed tomography. Successful surgery by replacement of the ascending aorta was performed about 1 h following admission to the intensive care unit. During the procedure, tamponade of the left ventricle occurred followed by cardiogenic shock. Postoperative management was complicated by prolonged respiratory therapy and acute gastrointestinal bleeding; 1-year follow-up showed no evidence of disease. Thus, in this case acute dissection may be the consequence of discontinuing the use of metoprolol, possibly due to uncontrolled hypertension or specific response to the beta-blocker.

Comparison of the effect of prostaglandin E1, prostacycline and adenosine on peripheral vascular resistance

Prostacycline, prostaglandin E1, and adenosine are highly effective vasodilators. These three drugs are widely used in the treatment of peripheral arterial occlusive disease. The aim of the study was to compare the vasodilatory potency of these substances in the isolated perfused guinea pig hind limb. After equilibration with Tyrodes solution and precontraction with noradrenaline 3µM, prostaglandin E1 and adenosine were administered at dosages of 0.1, 0.3, and 1µM, whereas prostacycline was administered at a dosage of 0.01, 0.03 and 0.1µM. 0.01µM prostacycline, 0.1 µM prostaglandin E1, and 0.1µM adenosine were the lowest dosages at which a significant vasodilation could be reached for each substance. The reduction of peripheral vascular resistance at comparable dosages of 0.1µM was 11.0 ± 2.6% (x ± SEM, n=5) for adenosine, 12.0 ± 1.0% (n=5) for prostaglandin E1, but 28.0 ± 9.3% (n=5) for prostacycline (p<0.05 versus adenosine and prostaglandin E1). Even at a dosage of 0.01 µM prostacycline, a comparable reduction in peripheral vascular resistance (16.0 ± 2.8%) could be reached, compared to a ten-fold higher dosage of prostaglandin E1 and adenosine. At the highest concentration of 1 µM, the vasodilatory effect of adenosine was significantly less expressed, compared to that of prostaglandin E1 (18.0 ± 3.4% versus 33.0 ± 4.7%). In summary, prostacycline, at a ten-fold lower concentration, showed comparable vasodilatory effects to adenosine and prostaglandin E1. The rank order at the vasodilatory potency is prostacycline > prostaglandin E1 > adenosine.

A high-resolution esophageal electrocardiogram for monitoring atrial activity in the hypothermic potassium-arrested heart.

Atrial electrical activities during hypothermic, K+-induced cardioplegic arrest correlate with an increased incidence of postoperative supraventricular dysrhythmias in coronary artery bypass graft patients. Surface electrocardiogram (ECG) (S-ECG) may be insufficiently sensitive to detect such activity intraoperatively, and invasive methods are impractical and traumatic. From induction of anesthesia until the end of surgery, esophageal ECG signals were detected with a new bipolar esophageal probe and a new high-resolution preamplifier (frequency range 0.01-2000 Hz). The S-ECG and the esophageal ECG (E-ECG) were evaluated independently in 18 patients. Eight of 18 patients presented during cardioplegic arrest a mean of 483 +/- 119 high-amplitude, biphasic P components (mean amplitude 0.7 +/- 0.1 mV, range 0.35-1.15 mV) per patient (mean 36 +/- 6 [5-59] potentials/min) similar to those coinciding with the surface ECG P-waves during sinus rhythm. Six of these eight patients presented a mean of 29 +/- 11 low atrial activities (mean amplitude 0.14 +/- 0.023 mV; range 0.1-0.25 mV) per patient (mean 8.4 +/- 5.6 [2.3-48] potentials/min) in the E-ECG. In the S-ECG, one patient of these eight presented 26 P waves during cardioplegic arrest simultaneously with activities in the E-ECG. During the first 5 days, seven of eight (88%) patients with atrial activities in the E-ECG versus 3 of 10 (30%) patients without atrial activities developed supraventricular tachyarrhythmias postoperatively (P < 0.05). This new high-resolution E-ECG device detected in a beat-to-beat technique more atrial activity during cardioplegic arrest than a S-ECG and offered the advantages of artifact exclusion and better prediction of postoperative supraventricular dysrhythmias. (Anesth Analg 1997;84:484-90)

Comparison of acute effects of anthracyclines on cardiac electrophysiological parameters of isolated guinea-pig hearts

SummaryThis study was performed to evaluate the acute effects of two anthracycline derivatives, doxorubicin and 4′O-tetrahydropyranyl-doxorubicin [(THP)-doxorubicin], on the conduction intervals, heart rate and refractoriness of isolated spontaneously beating guinea-pig hearts using a high-resolution ECG recording technique (SST-ECG). Doxorubicin as well as (THP)-doxorubicin were added to the perfusate in increasing concentrations of 0.1, 1 and 10 µm. Doxorubicin did not significantly alter the heart rate or conduction intervals. Only the rate-dependent QT interval was significantly shortened under the influence of 10 µm doxorubicin. In contrast, 10 µm (THP)-doxorubicin led to a significant reduction in the heart rate (−13% ± 3%;P <0.01,n = 7) and to a prolongation of atrioventricular conduction time (24% ± 10%;P <0.05,n = 7). The rate-dependent repolarization period (QT interval) was only insignificantly shortened in the presence of 10 µm (THP)-doxorubicin. The maximal following frequencies of each part of the conduction system were not changed by 10 µm doxorubicin. In the presence of (THP)-doxorubicin, the maximal following frequency of the ventricular myocardium was increased by as much as 36% ± 8% (P <0.01,n = 7), indicating a shortening of the effective refractory period of the ventricular myocardium (V-ERP). These results show that the activation of (THP)-doxorubicin resembles the effects of Ca-antagonistic compounds on the heart (i.e. decrease in the spontaneous sinus rate and prolongation of the AV-nodal conduction interval). Changes in the QT interval exerted by doxorubicin and the shortening of the ventricular effective refractory period by (THP)-doxorubicin may indicate an alteration of the K+-conductance of the membrane. As the acute electrophysiological effects of doxorubicin and (THP)-doxorubicin are modest and occur only at excessive concentrations (10 µm), a direct influence on the generation of arrhythmias in healthy hearts is unlikely.

Effect of Nifedipine and Verapamil on the Peripheral Resistance of Isolated Perfused Guinea Pig Hind Limbs

Arterial hypertension is a relevant concomitant disease in patients suffering from peripheral arterial occlusive disease (PAOD). At ages >65 years arterial hypertension is in second place with 58% after smoking as a risk factor for atherosclerosis [1]. This fact underscores the importance of antihypertensive treatment in patients with PAOD. For patients suffering from PAOD and hypertension it is important to choose antihypertensive drugs which have additional beneficial effects on peripheral circulation. Therefore, in the case of calcium antagonists, the question arises to what type of calcium antagonist decreases vascular resistance in the leg more, dihydropyredines or phenylalkylamines. In our study we chose two calcium channel blockers with different binding sites in the human body, namely nifedipine, a representative of the group of dihydropyredines, a mainly T-type channel blocker, and verapamil, a representative of the phenylalkylamine group, a mainly L-type channel blocker, and compared their effects on the vascular resistance of the isolated perfused guinea pig hind limb.