Interdisciplinary consensus on indications for transfemoral transcatheter aortic valve implantation (TF-TAVI) : Joint Consensus Document of the Arbeitsgemeinschaft Leitende Kardiologische Krankenhausärzte e.V. (ALKK) and cooperating Cardiac Surgery Departments.

Indications for TF-TAVI (transfemoral transcatheter aortic valve implantation) are rapidly changing according to increasing evidence from randomized controlled trials. Present trials document the non-inferiority or even superiority of TF-TAVI in intermediate-risk patients (STS-Score 4-8%) as well as in low-risk patients (STS-Score < 4%). However, risk scores exhibit limitations and, as a single criterion, are unable to establish an appropriate indication of TF-TAVI vs transapical TAVI vs SAVR (surgical aortic valve replacement). The ESC (European Society of Cardiology)/EACTS (European Association for Cardio-Thoracic Surgery) guidelines 2017 and the German DGK (Deutsche Gesellschaft für Kardiologie)/DGTHG (Deutsche Gesellschaft für Thorax-, Herz- und Gefäßchirurgie) commentary 2018 offer a framework for the selection of the best therapeutic method, but the individual decision is left to the discretion of the heart teams. An interdisciplinary TAVI consensus group of interventional cardiologists of the ALKK (Arbeitsgemeinschaft Leitende Kardiologische Krankenhausärzte e.V.) and cardiac surgeons has developed a detailed consensus on the indications for TF-TAVI to provide an up-to-date, evidence-based, comprehensive decision matrix for daily practice. The matrix of indication criteria includes age, risk scores, contraindications against SAVR (e.g., porcelain aorta), cardiovascular criteria pro TAVI, additional criteria pro TAVI (e.g., frailty, comorbidities, organ dysfunction), contraindications against TAVI (e.g., endocarditis) and cardiovascular criteria pro SAVR (e.g., bicuspid valve anatomy). This interdisciplinary consensus may provide orientation to heart teams for individual TAVI-indication decisions. Future adaptations according to evolving medical evidence are to be expected. Interdisciplinary consensus on indications for transfemoral transcatheter aortic valve implantation (TF-TAVI).

Laser angioplasty of restenosed coronary stents: results of a multicenter surveillance trial. The Laser Angioplasty of Restenosed Stents (LARS) Investigators.

OBJECTIVES: This study evaluated safety and efficacy of excimer laser angioplasty for treatment of restenosed or occluded coronary stents. BACKGROUND: Balloon angioplasty of in-stent restenosis is limited by a high recurrence rate. Debulking by laser angioplasty is a novel concept to treat in-stent restenosis. METHODS: A total of 440 patients with restenoses or occlusions in 527 stents were enrolled for treatment with concentric or eccentric laser catheters and adjunctive balloon angioplasty. RESULTS: Laser angioplasty success (< or =50% diameter stenosis after laser treatment or successful passage with a 2.0-mm or 1.7-mm eccentric laser catheter) was achieved in 92% of patients. Adjunctive balloon angioplasty was performed in 99%. Procedural success (laser angioplasty success followed by < or =30% stenosis with or without balloon angioplasty) was 91%. There was neither a significant difference in success with respect to lesion length, nor were there differences between small and large vessels or native vessels and vein grafts. Success was higher and residual stenosis lower using large or eccentric catheters. Serious adverse events included death (1.6%, not directly laser catheter related), Q-wave myocardial infarction (0.5%), non-Q-wave infarction (2.7%), cardiac tamponade (0.5%) and stent damage (0.5%). Perforations after laser treatment occurred in 0.9% of patients and after balloon angioplasty in 0.2%. Dissections were visible in 4.8% of patients after laser treatment and in 9.3% after balloon angioplasty. Reinterventions during hospitalization were necessary in 0.9% of patients; bypass surgery was performed in 0.2%. CONCLUSIONS: Excimer laser angioplasty with adjunctive balloon angioplasty is a safe and efficient technology to treat in-stent restenoses. These data justify a randomized comparison with balloon angioplasty.

Effects of chronic amiodarone therapy on defibrillation threshold.

In a prospective and parallel, randomized study, the long-term stability of epicardial defibrillation threshold was evaluated in 22 patients, using a patch-patch lead configuration at the time of implantation and generator replacement. The concomitant antiarrhythmic drug treatment consisted of either mexiletine (720 mg/day) or amiodarone (400 mg/day) and was administered to patients in a randomized and parallel manner. During a mean follow-up of 24 +/- 6 months, the defibrillation threshold increased significantly from 14.3 +/- 2.8 to 17.9 +/- 5.3 J (p < 0.05) for the entire patient group. The increase in the chronic defibrillation threshold was due to a marked increase in defibrillation energy needs in the subgroup of patients receiving amiodarone. Whereas no significant change in the defibrillation threshold was documented in the subgroup of patients receiving mexiletine, the mean defibrillation threshold increased from 14.1 +/- 3.0 to 20.9 +/- 5.4 J (p < 0.001) in those receiving amiodarone. In all patients with increased defibrillation thresholds, reevaluation showed a reduction in the defibrillation threshold after discontinuation of antiarrhythmic drug therapy. The only variable associated with an increase in the chronic defibrillation threshold was amiodarone treatment. These findings suggest that the defibrillation threshold should be measured at each generator replacement and in case of a change in antiarrhythmic drug treatment. In particular, if amiodarone treatment is initiated, it is recommended that the defibrillation threshold should be reevaluated to ensure an adequate margin of safety.

N-acetylcysteine attenuates nitroglycerin tolerance in patients with angina pectoris and normal left ventricular function.

The aim of this study was to assess whether N-acetylcysteine (NAC) is able to prevent tolerance to a 48-hour infusion of nitroglycerin (NTG) in the setting of normal left ventricular function. In 16 patients, the hemodynamic response to 0.8 mg sublingual (s.l.) NTG was assessed by measuring mean arterial, pulmonary artery, pulmonary capillary wedge and right atrial pressures, cardiac output, and calculation of the systemic and pulmonary vascular resistances. The parameters were obtained at baseline and 1 to 10 minutes after the s.l. NTG application (day 1). NTG was started at 1.5 microg/kg/min; concomitantly, a bolus of 2,000 mg of NAC was administered, followed by an infusion of 5 mg/kg/hour. Both infusions were continued for 48 hours, and the hemodynamic study was repeated (day 3). The same measurements were obtained in a matched control group of 15 patients with NTG infusion alone. Plasma renin activity, aldosterone, and norepinephrine were measured before and after the infusion period. The first s.l. NTG infusion (day 1) caused a significant decrease in mean arterial (p <0.01), pulmonary artery (p <0.001), and right atrial pressures (p <0.001), and in systemic (p <0.01) and pulmonary vascular resistances (p <0.001) in both groups. After the 48-hour infusion (day 3), there was a total loss of nitrate-mediated vasodilation (pressure values and vascular resistances day 3 > day 1) in 5 of 16 patients (NAC nonresponders), whereas in the other 11 of 16 patients (NAC responders), there was significant vasodilation throughout the infusion period. Tolerance had developed in 14 of 15 patients with NTG infusion alone. The same difference (responder vs nonresponder vs NTG alone) held true regarding the response to the second s.l. NTG infusion after 48 hours. The neurohormonal counter-regulation and intravascular volume expansion (increase in plasma renin activity, p <0.001, and norepinephrine, p <0.05; decrease in aldosterone, p <0.01) did not differ between responders and nonresponders. We conclude that NAC attenuates tolerance development to a continuous NTG infusion in a specific patient subgroup and that this occurs despite the same amount of neurohormonal counter-regulation and intravascular volume expansion compared with patients with tolerance development.

Paraprosthetic regurgitation in aortic prostheses: determination of the hemodynamic significance by pulsed Doppler examination of the subclavian artery flow.

Paraprosthetic leaks in aortic prostheses may cause significant aortic regurgitation. Color flow Doppler echocardiography is the method of choice for detecting paraprosthetic leaks, but quantitation of regurgitation is limited by this method. This study investigated the value of pulsed Doppler of the left subclavian artery flow for assessing the hemodynamic significance of paraprosthetic regurgitation in aortic prostheses in 32 patients with, and in 77 control subjects without paraprosthetic leaks. Paraprosthetic leaks were either detected by transthoracic or transesophageal color flow echocardiography. The hemodynamic significance of paraprosthetic regurgitation was determined by means of a dichotomous angiographic classification - significant versus insignificant regurgitation. Pulsed Doppler was performed to measure the maximal diastolic and systolic velocities, and diastolic and systolic velocity-time-integrals (VTI) and their ratios in the subclavian artery flow. The accuracy of these parameters for differentiating significant versus insignificant regurgitation was assessed. Angiography revealed 13 significant and 19 insignificant forms of aortic regurgitation. In all patients, examination of the subclavian artery was feasible by pulsed Doppler. The highest correlation between Doppler derived parameters and regurgitation was calculated for the ratios of diastolic and systolic VTI (r = 0.84), diastolic VTI (r = 0.82) and ratio of diastolic and systolic velocities (r = 0.80). An increase of the ratio of diastolic and systolic VTI (> 45%) and ratio of diastolic to systolic velocity (> 0.4), and increased diastolic VTI (> 60 cm) in the subclavian artery velocity profile identified significant paraprosthetic regurgitation with a sensitivity of 94%, 75% and 87%, and specificity of 87%, 80% and 87%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Valvular aortic stenosis: risk of syncope.

BACKGROUND AND AIMS: Syncope is a serious complication of aortic stenosis. The aim of this study was to determine whether hemodynamic parameters are useful for estimating the risk of syncope in aortic stenosis. METHODS: In 43 patients with aortic stenosis, cardiac catheterization and echocardiography were performed to measure the pressure gradient across the aortic valve, the aortic valve area, left ventricular mass index, systolic left ventricular wall stress and peak systolic coronary artery flow velocities. Hemodynamic parameters were correlated with syncope and the accuracy of those parameters for determining the risk of syncope were assessed. RESULTS: Ten out of 43 patients experienced syncope. The highest correlation with syncope was found for systolic left ventricular wall stress (R = 0.74, p < 0.001). In descending order of correlation were peak systolic coronary artery flow velocity (R = 0.68, p = 0.002), the pressure gradient across the aortic valve (R = 0.62, p = 0.01) and the aortic valve area (R = 0.43, p = 0.03). Left ventricular mass index was not significantly correlated with syncope. Multivariate analysis revealed systolic left ventricular wall stress to be the only factor contributing to determining syncope (F-to-remove: 47.8). A discriminative value of > 225 dyn/cm-2 x 103 for left ventricular wall stress identified patients with a history of syncope with a specificity of 97% and a sensitivity of 90%. CONCLUSIONS: Syncope in aortic stenosis is closely correlated to increased left ventricular wall stress and attenuated, peak systolic coronary flow velocities. Cut off values may be used to identify patients with an increased risk of syncope.

Inappropriate implantable defibrillator discharge caused by a retained pacemaker lead fragment.

INTRODUCTION: Inappropriate discharge is still a major issue of implantable cardioverter defibrillator therapy. The diagnostic options of modern devices facilitate classification of the underlying abnormality. METHODS AND RESULTS: A 65-year-old woman with depressed left ventricular performance received spurious shocks from an ICD, implanted for ventricular tachycardia. A lead fragment of an explanted VVI pacemaker system could be identified as cause of erroneous ventricular fibrillation detection by the ICD. The electrical noise caused by interaction between the lead remnant and the ICD lead was detectable even on the surface ECG. CONCLUSION: Based on our findings, removal of fragmented lead material should be considered prior to ICD implantation, to avoid potentially adverse and harmful interactions with ICD systems.

[Inhibition of the heparin effect by nitroglycerin]. / Hemmung der Heparinwirkung durch Glyceroltrinitrat.

The interaction of intravenous (i.v.) nitroglycerin (glyceryl trinitrate) on the anticoagulant effect of heparin was studied in 27 patients. The heparin dose was adjusted (800-1400 IU/h) to achieve partial thromboplastin time (PTT) of more than 100 s (130 +/- 28 s). While the heparin infusion was continued at the same dosage, the patients received 2-5 mg/h nitroglycerin i.v. (Perlinganit without propylene glycol [15 patients] or Gilustenon with propylene glycol [12 patients]). During combined heparin and nitroglycerin (NG) administration PTT decreased significantly (60 +/- 23 s; P less than 0.01). After withdrawal of NG, PTT increased to the initial levels (126 +/- 30 s). The drug interaction was seen in both groups--with or without propylene glycol. In nine of the 27 patients plasma heparin levels were measured; they remained unchanged during NG administration. The results indicate that i.v. NG induces heparin resistance. After NG is withdrawn, a rebound increase in PTT may occur. Adequate monitoring of PTT and heparin dosage adjustment are thus required during combined heparin and NG administration.

Mechanical dilatation rather than plaque removal as major mechanism of transluminal coronary extraction atherectomy.

Atherectomy with the transluminal extraction endarterectomy catheter (TEC) is a new approach for treatment of coronary artery disease, which continues to undergo FDA investigational studies. The major mechanism of the TEC device should be excision of plaque and its removal due to suction applied through an attached vacuum. We report about the acute results in 24 patients treated with TEC atherectomy in native vessels and the outcome of 18 patients who, until recently, underwent follow-up catheterization after 6 months. The procedure was successful (residual stenosis less than 50%) in 7 of 24 patients with TEC atherectomy alone (29%); 15 of 24 patients (65%) required additional PTCA in order to achieve angiographic success (10 of 24) or to treat total occlusion (2 of 24) or distal embolization (3 of 24) following atherectomy. One TEC attempt failed due to guiding catheter problems, another major complication was a vessel perforation leading to a non-Q wave infarction. The minimal residual diameter after passage of the stenosis (prior to additional PTCA) with the 5.5 Fr catheter (n = 14) was 1.5 +/- 0.2 mm, with the 6 Fr catheter (n = 9) 1.8 +/- 0.4 mm, and 2.2 +/- 0.2 mm using the 7 Fr catheter (n = 10). The histologic findings revealed intimal cells, fibrous tissue, and homogenate with no identifiable tissue in five cases (21%), whereas in 17 patients (72%) light microscopy could only assess blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in platelet size and count in unstable angina compared to stable angina or non-cardiac chest pain.

AIMS: An increase in platelet aggregability is associated with unstable angina and myocardial infarction. Platelet size and activity correlate and mean platelet volume was found to be increased before acute myocardial infarction. We measured the mean platelet volume and platelet count in patients with stable angina, unstable angina and non-cardiac chest pain. METHODS AND RESULTS: We studied 981 patients (734 men; 247 women) defined clinically as stable angina (n = 688), unstable angina (n = 108) and unstable angina requiring immediate angioplasty (n = 52). After coronary angiography the patients were subdivided into single (n = 269), double (n = 304) and triple-vessel disease (n = 311) and the control group of non-cardiac chest pain (n = 97). There was no significant difference in platelet count between the control group and patients with 1, 2, or 3-vessel disease. However, the platelet size in patients with coronary artery disease was significantly larger (single: 8.7 +/- 1.19 fl; double: 8.7 +/- 1.12 fl; triple-vessel disease: 8.8 +/- 1.18 fl) than the control group (8.2 +/- 0.95 fl) (P < 0.01). Patients with stable angina similarly had no, significant difference in platelet count compared to the control group but did have a significantly increased mean platelet volume (8.7 +/- 1.13; P < 0.01). In contrast, patients with unstable angina had a decreased platelet count (245 +/- 56 x 10/l) compared to either stable angina (262 +/- 62 x 10/l; P < 0.05) or the control group (261 +/- 58 x 10/l; P < 0.05); furthermore, the mean platelet volume (9.4 +/- 1.23 fl) was significantly greater than for stable angina (P < 0.01). Patients with unstable angina requiring immediate PTCA had an even lower platelet count (231 +/- 55 x 10/l) and higher mean platelet volume (10.4 +/- 1.03 fl) (P < 0.01) than the rest of the population with unstable angina. CONCLUSIONS: In stable angina the platelet count is unchanged compared to patients with normal coronary arteries but the platelet size is increased. However, in unstable angina there is a decrease in platelet count and an even larger increase in platelet size. We interpret this as meaning that unstable angina might be associated or preceded by an increase in platelet destruction rate that is not completely compensated for by an increase in platelet production rate. The large, more reactive platelets might be causally related to an ongoing coronary artery obstruction in unstable angina.

[Transluminal coronary extraction atherectomy. Method, acute results, angiographic and clinical follow-up]. / Transluminale koronare Extraktionsatherektomie. Methode, Akutergebnisse, angiographischer und klinischer Verlauf.

Transluminal coronary extraction-endarterectomy is an alternative interventional approach for treatment of coronary artery disease. The atherectomy system consists of a catheter assembly including a cutter and torque tube which is rotated at a relatively low rate of 750 rotations per minute, when introduced to the coronary artery over a guide-wire via a guiding catheter. Excised tissue is withdrawn from the coronary artery by suction applied through the catheter by means of an attached vacuum bottle. We report acute results in 18 patients and the clinical outcome of 14 patients who up to now underwent angiographic follow-up catheterization after 6 months. Initial angiographic success (residual stenosis less than 50%) using TEC-atherectomy alone was obtained in 6/18 patients (33%), 11/18 patients (60%) required additional PTCA in order to achieve primary success (9/18) or to treat total occlusion (2/18) after TEC-atherectomy. Major complications consisted in 1-vessel perforation with non-Q-wave-infarction but no need of surgical intervention and 2 occlusions due to dissection (treated with PTCA). 14 patients underwent angiographic follow-up (6 months) and restenosis (greater than 50%) was confirmed in 7 patients (50%). Considering the low primary success rate of TEC-atherectomy alone and the tendency to high restenosis rate, we cannot recommend it as an alternative to conventional PTCA in general clinical practice. Further studies should be designed to directly compare TEC-atherectomy to PTCA in specific patient subgroups (e.g. bypass grafts, intraluminal thrombus, diffuse disease) in order to define the role of this interventional device.

Prognostic analysis and predictive rule for outcome of hospital-treated community-acquired pneumonia.

In community-acquired pneumonia (CAP) mortality may be reduced by early identification of patients requiring intensive care treatment. The purpose of this study was to determine prognostic factors of outcome in patients with CAP in order to establish a clinically applicable discriminant rule. Ninety three episodes of CAP in 92 patients were retrospectively reviewed with regard to epidemiological, clinical, laboratory and microbiological data. The prognostic analysis included a univariate as well as a multivariate approach, in order to identify parameters associated with death using the Cox regression hazard function in a backward stepwise selection model. The three parameters found to contribute most to the significance of the model were used in a discriminant rule for classification of outcome. The parameters found to be significantly different between survivors and non-survivors were heart rate, systolic and diastolic as well as mean blood pressures, leucocyte count, percentage of lymphocytes, and lactate dehydrogenase (LDH) values. The multivariate analysis revealed that heart rate, systolic arterial pressure, and LDH serum levels were most closely associated with fatal outcome. A prognostic rule composed of the variables heart rate > or = 90 beats.min-1, systolic arterial blood pressure < or = 80 mmHg, and LDH > or = 260 U.l-1 achieved a sensitivity of 77%, a specificity of 75%, and positive and negative predictive values of 42 and 93%, respectively. It was associated with a six fold increased risk of fatal outcome. In conclusion, heart rate, systolic blood pressure, and LDH values were most closely associated with death in a multivariate analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Influence of captopril on nitroglycerin-mediated vasodilation and development of nitrate tolerance in arterial and venous circulation.

We investigated whether captopril is able to potentiate vasodilation and prevent tolerance to a 48-hour infusion of nitroglycerin (NTG). Twenty-six patients were randomly assigned to a 7-day regimen of captopril (50 mg/day) or placebo. The hemodynamic response to a 0.8 mg sublingual NTG dose was assessed by measuring mean arterial pressure (MAP), mean pulmonary artery pressure (PAP), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), and cardiac output (CO), and calculating systemic (SVR) and pulmonary vascular resistances (PVR). The parameters were obtained serially at baseline and 1 to 10 minutes after the sublingual NTG application (day 1). Then intravenous NTG was started and maintained for 48 hours (1.5 micrograms/kg/min), and the hemodynamic study was repeated (day 3). There was no difference between the captopril and the placebo groups at day 1 (baseline values and response to sublingual NTG). After the 48-hour infusion, there was a complete loss of the NTG effects in the placebo group (day 1 vs day 3: PAP, 20 +/- 5 mm Hg vs 21 +/- 8 mm Hg; MAP, 86 +/- 11 mm Hg vs 90 +/- 9 mm Hg; SVR, 1295 +/- 330 mm Hg vs 1380 +/- 465 dyne.sec.cm-5) whereas there was still evidence of a persistent vasodilation in the captopril group (day 1 vs day 3: PAP, 19 +/- 4 mm Hg vs 13 +/- 4 mm Hg; MAP, 84 +/- 9 mm Hg vs 74 +/- 10 mm Hg; SVR, 1265 +/- 280 mm Hg vs 1140 +/- 425 dyne.sec.cm-5). The response to sublingual NTG on day 3 was markedly attenuated in the placebo group only. We conclude that captopril does not increase the vasodilatory response to nitroglycerin but is able to prevent developing nitrate tolerance in arterial and venous circulation.

Clinical characteristics and outcome of Pneumocystis carinii pneumonia in HIV-infected and otherwise immunosuppressed patients.

The factors contributing to unequal mortality rates following Pneumocystis carinii pneumonia (PCP) in different groups at risk are poorly understood. We therefore compared the first episodes of PCP without prophylaxis in human immunodeficiency virus infected (HIV) and otherwise immunosuppressed patients in this retrospective study. A total of 58 HIV-infected and 16 otherwise immunosuppressed patients were analysed. The comparison included epidemiological, clinical, laboratory, radiological and microbiological data, as well as therapy and clinical course. A prognostic analysis was performed using a logistic regression model. The mortality was significantly different in the two groups (HIV group 17 versus non-HIV group 50%). Renal transplant patients had a higher survival rate as compared to malignancy or collagen vascular disease as underlying diseases at risk. Acute respiratory failure was more common in the non-HIV group. Variables found to be significantly associated with lethal outcome in univariate analysis were alveolar to arterial pressures difference for oxygen (P(A-a),O2), haemoglobin, platelet count, total protein, serum albumin, and gamma-globulins in the HIV-group, and serum albumin in the non-HIV group. In the multivariate analysis of the HIV group, platelet count and gamma-globulins remained independent prognostic factors. In conclusion, in the HIV-group, mortality is closely related to the severeness of PCP as well as to the severeness of the acquired immune deficiency syndrome (AIDS) disease. In the non-HIV group, malignancy and collagen vascular disease as underlying conditions at risk account for the high mortality rate. Its severeness was mainly reflected by serum albumin, which represented the only variable found to be significantly associated with death in both groups.

Time course of myocardial and cerebral blood flow during stable but hemodynamically compromising ventricular tachycardias. Laboratory investigations.

Myocardial and cerebral blood flow were determined with radiolabeled microspheres in 20 Sprague-Dawley rats during sinus rhythm and during stable but hemodynamically compromising ventricular tachycardias. In addition, in 10 animals the measurements were performed at hypotension induced by exsanguination. In controls (n = 10), myocardial and cerebral blood flow were 5.14 +/- 0.6 and 1.03 +/- 0.3 ml/g per minute, respectively. The range of myocardial blood flow values was markedly enlarged after onset of tachycardia induced by epicardial pacing. The mean values of myocardial blood flow were 5.80 +/- 1.9 ml/g per minute (n.s.) after 1 min and 7.46 +/- 3.9 ml/g per minute (n.s.) after 5 min. Cerebral blood flow, however, significantly decreased after 1 min (0.57 +/- 0.1 ml/g per minute, P < 0.01) and after 5 min (0.71 +/- 0.3 ml/per minute, P < 0.05). In contrast, 1 min after exsanguination myocardial blood flow significantly decreased (4.03 +/- 1.5 ml/g per minute, P < 0.05) and recovered after 5 min (6.06 +/- 1.2 ml/g per minute, n.s.) Cerebral blood flow was below control levels 1 min (0.70 +/- 0.2 ml/g per minute, P < 0.05) after onset of hypotension due to exsanguination and returned to normal values with the next 4 min (0.90 +/- 1 ml/g per minute, n.s.). The results suggest that stable but hemodynamically compromising ventricular tachycardias markedly affect cerebral blood flow, whereas in most cases myocardial blood flow is maintained within normal ranges, or even increases. An augmented myocardial autoregulation can be concluded from the autoregulatory index. This maintainance of regulatory ability might be due to the increase of myocardial oxygen consumption at decreased coronary perfusion pressure during tachycardias. In contrast, during hypovolemic hypotension, myocardial as well as cerebral blood flow decreased. During stable but hemodynamically compromising ventricular tachycardias, cerebral blood flow initially drops drastically and recovers slowly over the next 5 min. This finding contrasts with the results of hypovolemic and drug-induced hypotension models.

[Effect of nisoldipine and diltiazem on systolic and diastolic function of the left ventricle in patients with coronary heart disease]. / Der Einfluss von Nisoldipin und Diltiazem auf die systolische und diastolische Funktion des linken Ventrikels bei Patienten mit koronarer Herzkrankheit.

OBJECTIVES AND BACKGROUND: Calcium channel blockers have a negative inotropic effect and protract the relaxation of the normal myocardium. These effects may vary in patients with coronary artery disease (CAD) and with the different kinds of calcium antagonists. In the present study we therefore compared the hemodynamic effects of intravenously given equihypotensive dosages of diltiazem (D) and nisoldipine (N) in patients with CAD. METHODS AND RESULTS: Each group contained 10 patients. After administration of a bolus of 300 micrograms/kg (D) and 5 micrograms/kg (N) respectively and following continuous infusion of 5.4 micrograms/kg/min (D) and 0.2 micrograms/kg/min (N) respectively, the mean arterial pressure was reduced by 15.5 +/- 6.0 (D) and 16.6 +/- 4.1 (N) mm Hg. Atrial pacing was performed in all patients to avoid reflectory heart rate effects. The pulmonary artery pressure decreased slightly with both drugs, whereas the cardiac index increased only with the use of N from 3.44 l/min x m2 to 3.93 l/min x m2. A significant change in the maximal rate of rise of left ventricular pressure (dP/dt max) as an index for inotropy was not detected for N or for D. The parameters of the diastolic function (the time constant of ventricular relaxation (tau) and the maximum rate of left ventricular isovolumic pressure decline (dP/dt min)) also did not indicate unequivocal drug effects. Doppler echocardiography of the mitral valve flow was performed simultaneously with invasive pressure measurements. The flow propagation derived from the color-M-mode correlated significantly with tau and was slightly improved by D.(ABSTRACT TRUNCATED AT 250 WORDS)

Percutaneous extraction of an abandoned coiled pacing lead.

Abandoning redundant pacing leads has been an accepted practice in most cases. Late migration of a lead is a rare, unpredictable, and potentially lethal complication of this approach and requires immediate removal. We report the case of an atrial pacing lead that had migrated and was found coiled in the right atrium. It was removed by a snare catheter via a femoral approach.

[Catheter ablation as an emergency treatment in Wolff-Parkinson-White syndrome with signs of acute infarct]. / Katheterablation als Notfalleingriff bei Wolff-Parkinson-White-Syndrom mit akuten Infarktzeichen.

A 53-year-old man known to have Wolff-Parkinson-White syndrome suffered an acute posterior-wall myocardial infarction. Despite successful thrombolysis treatment with streptokinase he continued to have attacks of supraventricular tachycardia with angina. The ECG showed a short P-R interval and pre-excitation with positive delta waves in leads V1-6, as well as signs of re-infarction. The tachycardias could not be satisfactorily suppressed by drug treatment. Coronary angiography revealed triple vessel disease. During this investigation ventricular extrasystoles occurred which initiated orthodromic supraventricular tachycardia and angina, as well as monophasic S-T elevations in leads II, III and aVF. This provided the indication for immediate high-frequency catheter ablation left laterally at the mitral anulus after a left-lateral accessory conduction pathway had been identified. Three days later the stenoses of the circumflex and anterior interventricular branches were dilated. The patient has been free of symptoms for 3 months and can exercise up to 150 W. The tachycardias have not recurred.