Biomedical subjects
Publications and source records attributed to G V Sabin.
This paper reports in detail on a project of Integrated Health Care in cardiology at Essen, Germany. Information on the structure of the contract, the participants, the agreed claiming of benefits and provision of services are provided as well as relevant figures and contact data.
The German "GKV-Modernisierungsgesetz" offers new opportunities for patient care. The concept of "integrated care" provides organizational structures for an standardized treatment of myocardial infarction by bridging the different sectors of the German health care system. Apart from guideline-based therapy, innovative diagnostic (cardiac MRI) and therapeutic (drug-eluting stents) techniques are implemented in the "integrated care" model as well. The "Herzinfarktverbund Essen" is the first national real world experience of the integrated care concept in the treatment of myocardial infarction.
PURPOSE: Transthoracic echocardiography is the routine diagnostic procedure in assessing patients with left ventricular thrombi, but is limited by the acoustic window and poor contrast between thrombus and adjacent myocardium. This study evaluates the role of cardiac MRI in the detection of left ventricular thrombi in patients with chronic myocardial infarction compared to standard transthoracic echocardiography. MATERIALS AND METHODS: In 82 patients (55 men and 27 women, age 36 to 79 years, median 59 +/- 11 years) who suffered a myocardial infarction more than 6 months earlier, transthoracic echocardiography and MRI were performed. The MRI protocol included steady state cine imaging (true FISP: TR 3.0 ms, TE 1.5 ms, FA 65 degrees ) in standard long and short axis orientation and contrast-enhanced imaging using a 3D IR-FLASH sequence with long inversion time (TR 4 ms, TE 1.43 ms, FA 10 degrees , TI 300 ms) early, and a 2D IR-FLASH sequence with optimized inversion time (TR 8 ms, TE 4.3 ms, FA 20 degrees , TI 180 - 280 ms) late after administration of gadolinium. RESULTS: Transthoracic echocardiography depicted 12 thrombi. Contrast-enhanced MRI confirmed these 12 thrombi and detected 23 additional thrombi. With the exception of 2 very small apical thrombi only visible on contrast-enhanced MR images, spherical thrombi were diagnosed by both techniques, whereas only contrast-enhanced MRI was able to visualize mural thrombi. Left ventricular thrombi were more frequently diagnosed in patients with moderate to severe impairment of the left ventricular systolic function, 32/42 (76 %), or in patients with left ventricular aneurysms, 21/24 (84 %). CONCLUSION: Contrast-enhanced MRI is mostly superior to transthoracic echocardiography in diagnosing mural left ventricular thrombi in patients who had suffered a myocardial infarction. Intracavitary thrombi are more frequently found in patients with impaired regional and global left ventricular function.
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AIM: Purpose of our study was to compare the image quality of 3D-navigator steady state free precession (SSFP) and gradient echo (GE) sequences for magnetic resonance coronary angiography (MRCA) in volunteers and patients. METHODS: Following informed consent 8 volunteers and 12 patients were included into this study. In all subjects a 3D navigator MRCA of the right and the left coronary artery was performed with a SSFP (TR 3.9 ms, TE 1.7 ms, FA 65 degrees, bandwidth 540 Hz) and a GE (TR 5.8 ms, TE 2.2 ms, FA 25 degrees, bandwidth 200 Hz) sequence using a 1.5 T-MR-System (Magnetom Sonata, Siemens Erlangen). The slice thickness was 1.5 mm and the in-plane resolution was 0.9 x 0.7 mm (2) for all measurements. RESULTS: The blood pool showed a significantly (p < 0.01) higher signal intensity on SSFP images (147 +/- 36) compared to GE images (103 +/- 36). Although noise increased with SSFP (9.3 +/- 1.4 versus 5.3 +/- 0.9), the contrast-to-noise ratio between myocardium and the coronaries was significantly (p < 0.01) higher on SSFP images (7.8 +/- 3.7 versus 3.4 +/- 3.3). The CNR between the coronaries and the epicardial fat showed no significant differences (12 +/- 5 versus 13 +/- 4). CONCLUSION: The 3D-navigator SSFP sequence is a promising new technique for MRCA which improves the contrast between the coronaries and the myocardium and shortens the data acquisition compared to gradient-echo imaging.
Acquired muscular ventricular septal defects (MVSD) after myocardial infarction (MI) can lead to right heart failure and cardiogenic shock with high mortality. Early surgical therapy is often difficult to perform but can reduce the mortality. The closure of congenital septal defects is performed with high safety. Therefore, the interventional closure of an acquired post-MI VSD might be feasible and of potential benefit. To date, experiences with closure of post-MI MVSDs are minimal. We report on two patients with post-MI VSD.
AIM: Most atrioventricular accessory pathways (AV-APs) exhibit Kent bundle physiology characterized by fast and non-decremental conduction properties. In contrast, atriofascicular APs, which are only capable of reaching slow levels of long antegrade decremental conduction, are uncommon. The aim of this study was to describe antegrade and/or retrograde AV-APs with unusual decremental properties. METHODS AND RESULTS: Five patients with unusual decremental AV-APs underwent electrophysiological evaluation and radiofrequency catheter ablation for symptomatic tachycardias. Three were found to have structural heart disease, and three latent decremental AV-APs in the anterograde and/or retrograde direction that could not be demonstrated by routine electrophysiological testing. In Case 1, a right posteroseptal AV-AP with bidirectionally latent decremental conduction was associated with clinical antidromic circus movement tachycardia (CMT) mimicking ventricular tachycardia and orthodromic CMT, the latter inducible only with isoprenaline. In Case 2, incessant orthodromic CMT was due to a latent retrograde left posterolateral AV-AP. In both cases, double atrial responses to a single paced ventricular beat, initiating orthodromic CMT, were observed. In Case 3 with latent preexcitation unmasked by adenosine and atrial pacing, retrograde latent decremental conduction over a right posteroseptal AV-AP could be shown only with isoprenaline. This patient and the remaining two with overt preexcitation demonstrated anterograde decremental AP conduction that was discontinuous over a right posteroseptal AV-AP in Cases 3 and 4 and was continuous over a midseptal AV-AP in Case 5. In the latter case, the site of decremental conduction could be localized at the proximal AP origin. All five AV-APs were successfully ablated at the annulus level. CONCLUSION: AV-APs with unusual decremental properties that are either latent, demonstrable only during CMT or overt, exhibiting functional longitudinal dissociation are described. These APs could be identified and successfully ablated after detailed electrophysiological analysis.
INTRODUCTION: True nodoventricular or nodofascicular pathways and left-sided anterograde decremental accessory pathways (APs) are considered rare findings. METHODS AND RESULTS: Two unusual patients with paroxysmal supraventricular tachycardia were referred for radiofrequency (RF) ablation. Both patients had evidence of dual AV nodal conduction. In case 1, programmed atrial and ventricular stimulation induced regular tachycardia with a narrow QRS complex or episodes of right and left bundle branch block not altering the tachycardia cycle length and long concentric ventriculoatrial (VA) conduction. Ventricular extrastimuli elicited during His-bundle refractoriness resulted in tachycardia termination. During the tachycardia, both the ventricles and the distal right bundle were not part of the reentrant circuit. These findings were consistent with a concealed nodofascicular pathway. RF ablation in the right atrial mid-septal region with the earliest atrial activation preceded by a possible AP potential resulted in tachycardia termination and elimination of VA conduction. In case 2, antidromic reciprocating tachycardia of a right bundle branch block pattern was considered to involve an anterograde left posteroseptal atriofascicular pathway. For this pathway, decremental conduction properties as typically observed for right atriofascicular pathways could be demonstrated. During atrial stimulation and tachycardia, a discrete AP potential was recorded at the atrial and ventricular insertion sites and along the AP. Mechanical conduction block of the AP was reproducibly induced at the annular level and at the distal insertion site. Successful RF ablation was performed at the mitral annulus. CONCLUSION: This report describes two unusual cases consistent with concealed nodofascicular and left anterograde atriofascicular pathways, which were ablated successfully without impairing normal AV conduction system.
Heparin-induced thrombocytopenia type II (HIT type II) is the most serious complication of heparin treatment apart from bleeding, which is the most common side effect. Eleven days after coronary bypass grafting, a 71 year old patient showed a posterolateral myocardial infarction and a thrombocytopenia of 80,000/microliter. This was considered a postoperative thrombocytopenia. Coronary angiography revealed closed venous bypass grafts. The right coronary artery (RCA) was revascularized by percutaneous transluminal coronary angioplasty (PTCA) and stent placement. During both coronary angiography and PTCA, heparin was administered to the patient. The platelet number did not change. Four days later the patient showed an inferior myocardial infarction and an AV-block III degrees and a syncope. The following coronary angiography revealed RCA stent occlusion. HIT type II was presumed and recanalization was carried out using Lepirudin (Refludan) as the anticoagulant. After placing the guide wire, thrombi could be seen in the proximal RCA. Abciximab (Reo pro), a monoclonal antibody against the glycoprotein IIb/IIIa receptor was additionally administered. Coronary angiography on the next day revealed only a small remaining thrombus. The AV-block disappeared immediately after revascularization. The diagnosis of HIT type II was confirmed through heparin-induced-platelet-activation-test (Hipa-test) and immunoassay (PF 4/heparin-ELISA). This case report illustrates the complicated diagnosis of HIT type II and the successful simultaneous use of Lepirudin (Refludan) and Abciximab (Reo pro). The number of platelets should be checked daily during heparin treatment. In the case of a thrombocytopenia, the treatment should be stopped immediately, and Hipa-test and PF 4/heparin-ELISA should be carried out.
INTRODUCTION: We present the case of a 17-year-old woman who underwent an electrophysiological study and radiofrequency (RF) ablation of supraventricular tachycardia refractory to medical treatment. Two right-sided, concealed, nondecremental atrioventricular accessory pathways (AV-APs) involved in orthodromic circus movement tachycardias were identified. After RF ablation of both AV-APs, evidence of bidirectional dual AV nodal conduction was demonstrated and regular narrow complex tachycardia was induced. METHODS AND RESULTS: During the tachycardia, retrograde slow and fast AV nodal pathway conduction with second-degree ventriculoatrial (VA) block and VA dissociation were observed. During the tachycardia with second-degree VA block, ventricular extrastimuli elicited during His-bundle refractoriness advanced the next His potential or terminated the tachycardia. Mapping the right atrial mid-septal region, a distinct high-frequency activation P potential was recorded in a discrete area, two thirds of the way from the His bundle toward the os of the coronary sinus. Detailed electrophysiologic testing with the recordable P potential demonstrated that the tachycardia utilized a concealed nodoventricular AP arising from the proximal slow AV nodal pathway. CONCLUSION: The tachycardia with slow 1:1 VA conduction could be reset by ventricular extrastimuli elicited during His-bundle refractoriness advancing the subsequent activation P potential and atrial activation. RF ablation guided by recording of the activation P potential resulted in elimination of both the slow AV nodal pathway and the nodoventricular connection with preservation of the normal AV conduction system.
HISTORY AND CLINICAL FINDINGS: A 39-year-old woman complained of dyspnoea and increasing abdominal pressure sensation. A Greenfield filter had been implanted into her inferior vena cava (IVC) 4 years previously because of pulmonary embolism from a deep vein thrombosis after a hysterectomy with abscess formation. Physical examination revealed neck vein congestion, jaundiced sclerae, a tense abdominal wall, ascites and a soft machinery murmur in the paraumbilical region. INVESTIGATIONS: Transaminase activities were slightly raised (GOT 38 U/I, GPT 20 U/I), but total bilirubin and direct bilirubin were markedly elevated (2.9 mg/dl and 1.1 mg/dl, respectively). There was no evidence of cholestasis or decreased liver synthesis. Ultrasound showed marked dilatation of the IVC and hepatic veins, and echocardiography revealed right ventricular enlargement with grade II tricuspid regurgitation. Calculated pulmonary arterial systolic pressure averaged 50 mmHG. Colour-coded Doppler sonography demonstrated an aorto-caval shunt at the level of the filter in the IVC and penetration of a filter strut into the aortic lumen. TREATMENT AND COURSE: After removing the ascitic fluid by fluid and sodium restriction, and administration of an aldosterone antagonist and a loop diuretic, the A-V fistula was closed surgically and the filter removed. Three months after operation she was put on phenprocoumon (Quick value 20-30%). At the latest outpatient examination, 6 months after the operation, she was free of symptoms. CONCLUSION: As filter implantation in the IVC may produce severe complications, indications for it need to be demonstrated by further studies of its efficacy.
Early action of angiotensin-converting enzyme (ACE) inhibitors after myocardial infarction (MI) has been shown in large scale clinical trials to reduce mortality over the first weeks. However, the mechanisms involved are yet unclear and several trials showed a tendency toward a small, albeit unexpected, rise in cardiogenic shock or mortality. Since cardiopulmonary exercise testing (CPX) has become a "gold standard" in assessing the severity of heart failure, we studied--after finishing a pilot trial--the effect of captopril versus placebo in 208 patients who were individually titrated (titrated dose, mean 46/69 mg/day after 7 days/4 weeks, respectively) in order to preserve their blood pressure in the acute phase of myocardial infarction; we followed the development of congestive heart failure (CHF) over 4 weeks by measuring oxygen consumption. After 4 weeks, overall oxygen consumption at the anaerobic threshold (VO2-AT; 13.7 vs 13.1), maximal oxygen consumption (VO2max 19.3 vs 18.9 mL/kg per min) and exercise duration (896 vs 839 sec) showed a nonsignificant difference in favor of the captopril group. The predefined, categorized, combined endpoint of severe heart failure or death (heart failure necessitating ACE inhibition, VO2max < 10 mL/kg per min, or death) was significantly reduced in the captopril group (n = 7/104) versus placebo (n = 18/104; p = 0.03). Differences were mainly caused by fewer CHF events (delta n = 10). We conclude that ACE inhibition with individualized dose titration markedly reduces the 4-week incidence of severe heart failure or death; > 10 patients per 100 treated gained major benefits from this therapy.
This paper reports the case of a 63-year-old female patient with Wolff-Parkinson-White syndrome who underwent an electrophysiologic study (EPS) and ablation using temperature-guided radiofrequency current for atrial fibrillation with a shortest preexcited RR interval of 160 ms. Detailed EPS and mapping demonstrated an unusual, complex left-sided accessory pathway, with the two distinct branches having two remote atrial insertions and a narrow common ventricular isthmus associated with the manifestation of atrial double potentials recorded from the coronary sinus. Simple ablation at the left lateral side from the ventricular aspect completely eliminated complex accessory pathway conduction, resulting in the disappearance of atrial double potentials.
1. PD 81,723 has been shown to enhance binding of adenosine to A1 receptors by stabilizing G protein-receptor coupling ('allosteric enhancement'). Evidence has been provided that in the perfused hearts and isolated atria PD 81,723 causes a sensitization to adenosine via this mechanism. 2. We have studied the effect of PD 81,723 in guinea-pig isolated atrial myocytes by use of whole-cell measurement of the muscarinic K+ current (I[K(ACh)]) activated by different Gi-coupled receptors (A1, M2, sphingolipid). PD 81,273 caused inhibition of I[K(ACh)] (IC50 approximately 5 microM) activated by either of the three receptors. Receptor-independent I[K(ACh)] in cells loaded with GTP-gamma-S and background I[K(ACh)], which contributes to the resting conductance of atrial myocytes, were equally sensitive to PD 81,723. At no combination of concentrations of adenosine and PD 81,723 could an enhancing effect be detected. 3. The compound was active from the outside only. Loading of the cells with PD 81,723 (50 microM) via the patch pipette did not affect either I[K(ACh)] or its sensitivity to adenosine. We suggest that PD 81,723 acts as an inhibitor of inward rectifying K+ channels; this is supported by the finding that ventricular I(K1), which shares a large degree of homology with the proteins (GIRK1/GIRK4) forming I[K(ACh)] but is not G protein-gated, was also blocked by this compound. 4. It is concluded that the functional effects of PD 81,723 described in the literature are not mediated by the A1 adenosine receptor-Gi-I[K(ACh)] pathway.
This report describes the case of a 19-year-old patient with Ebstein's anomaly, who had an unusual combination of a right atriofascicular (Mahaim) and two ipsilateral right atrioventricular (Kent) accessory pathways participating in three types of antidromic and orthodromic reciprocating tachycardias in the absence of retrograde conduction over the bundle of His-atrioventricular node axis. All three pathways were ablated in a single session using temperature-guided radiofrequency current.
An electrophysiologic study of atrial tachycardia is presented. During tachycardia, transient entrainment and sinus rhythm, two patterns of persistent double potentials in the high right atrium and fragmented activity in the low atrial septum were observed. No activity was recorded from multiple areas of the right atrium with endocardial mapping during sinus rhythm. The observations suggest that persistent fragmented activity represents slow conduction within the circuit which could be orthodromically entrained. Persistent double potentials probably represent slow conduction orthodromically and/or antidromically activated outside the circuit. However, a wave front from pacing impulses travelling through this area could entrain the circuit.
Left ventricular damage by necrosis of myocardial tissue can lead to compromise of left ventricular function, to left ventricular volume increase and ultimately to development of heart failure. This sequence in the pathophysiology has been shown to be blunted by ACE inhibitors. Volume increase, however, can also be helpful in restoring stroke volume and ameliorate elevation of filling pressures. Furthermore, very early institution of ACE inhibition has failed to improve short-term mortality after myocardial infarction in one large trial. The aim of the ECCE trial therefore is, to investigate the early effects of the ACE inhibitor captopril on compromise of exercise capacity, thought to be a first measurable sign of developing heart failure. The ECCE trial is a randomized, seven-center investigation, studying the effects of ACE inhibition on oxygen uptake in a double blind, placebo controlled design in a group of 204 patients. Sample size was calculated on the basis of a pilot trial. The study design and first not unblinded data of 104 patients are presented. The population consists of predominantly male patients with mostly first myocardial infarction. They were admitted to hospital within five hours of onset of chest pain. End-diastolic volumes were normal, but ejection fraction was moderately compromised. ACE inhibition was started after the first day, but within 72 hours of onset of chest pain. After four and after twelve weeks, oxygen uptake was considerably below expected values and one third of the patients had severe compromise of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)
Ibopamine is an active dopamine analogue leading to improved renal perfusion and afterload reduction in heart failure. This report describes casuistic experiences in patients with severe heart failure awaiting heart transplantation. All patients could be stabilized, intravenous catecholamines be discontinued, and diuretics be reduced. Six of seven patients could be successfully transplanted. No major side effects were noted. Thus ibopamine can be a suitable adjunct for patients with endstage heart failure.