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Biomedical subjects

M Roelke

Publications and source records attributed to M Roelke.

36 records · Page 2Linked to original sources

Limitations and late complications of third-generation automatic cardioverter-defibrillators.

BACKGROUND: This study examines the limitations and complex management problems associated with the use of tiered-therapy, implantable cardioverter-defibrillators (ICDs). METHODS AND RESULTS: The study group comprises the first 154 patients undergoing implantation of tiered-therapy ICDs at our institution. Pulse generators from three different manufacturers were used. In 39 patients, a complete nonthoracotomy lead system was used. The perioperative mortality was 1.3%. Of these 154 patients, 37% experienced late postoperative problems. Twenty-one patients required system revision within 36.5 months (mean, 8.57 +/- 11.3) of surgery. Reasons for revision were spurious shocks due to electrode fractures (3) or electrode adapter malfunction (2), inadequate signal from endocardial rate-sensing electrodes (3), superior vena cava or right ventricular coil migration (5), failure to correct tachyarrhythmias due to a postimplant rise in defibrillation threshold (5), or pulse generator failure (3). One of these patients required system removal for infection after revision of an endocardial lead. A further 32 patients received inappropriate shocks for atrial fibrillation with a rapid ventricular response or sinus tachycardia. Two of these patients also received shocks for ventricular tachycardia initiated by antitachycardia pacing triggered by atrial fibrillation. Ventricular pacing for bradycardia was associated with inappropriate shocks due to excessive autogain in 2 patients. CONCLUSIONS: Despite the major diagnostic and therapeutic advantages of tiered-therapy ICDs, a significant proportion of patients continue to experience hardware-related complications or receive inappropriate shocks.

Algorithms↗

Electrocardiographic pseudo-infarct patterns after implantation of cardioverter-defibrillators.

Postoperative electrocardiographic (ECG) changes are frequently present after insertion of implantable cardioverter-defibrillators (ICD) and may mimic perioperative myocardial infarction (MI). The purpose of this study was to assess the incidence and clinical significance of postoperative ECG changes in relation to clinical, laboratory, and implantation data. In 25 (16%) of 156 patients undergoing ICD implantation, significant ECG changes (> or = 50% reduction in R-wave amplitude in > or = 3 leads or new Q waves in > or = 2 leads) were present 1 to 3 days after the operation and persisted at hospital discharge in 12 (8%). Presence of thoracotomy, the total number of induced ventricular fibrillation episodes, and the number of defibrillation shocks required during defibrillation threshold (DFT) testing correlated with postoperative ECG changes. Other factors associated with a significant R-wave loss in the lateral precordial leads included left-sided pleural effusion, lung infiltrates or atelectasis, and large defibrillator patch electrodes over the left ventricle or the lateral chest wall. Myocardial necrosis documented by elevated cardiac enzymes occurred in 6 (5%) of 151 patients without significant ECG changes and in 3 (12%) with (p value not significant). However, postoperative ECG changes associated with elevated enzymes were indistinguishable from changes unrelated to necrosis. Therefore the sensitivity and specificity of the surface ECG for detection of MI after ICD placement is poor. Multiple factors such as thoracotomy, myocardial injury from DFT testing, electric insulation, or shielding of the heart may contribute to the development of electrocardiographic pseudo-infarct patterns.

Aged↗

Ventricular pacing induced ventricular tachycardia in patients with implantable cardioverter defibrillators.

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 +/- 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1-16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.

Aged↗

Subclavian crush syndrome complicating transvenous cardioverter defibrillator systems.

UNLABELLED: Subclavian crush syndrome, described with pacemaker leads implanted via subclavian puncture, may occur when conductor fractures and insulation breaches develop by compression of a lead between the first rib and clavicle. We reviewed our experience in 164 patients who underwent intended implantation of transvenous defibrillator systems to determine the clinical relevance of subclavian crush syndrome in defibrillator patients. Venous access was obtained via subclavian puncture in 114 patients (70%) and via cephalic cut-down in 50 patients (30%). Nonthoracotomy lead systems, with or without subcutaneous patch, were successfully implanted in 131 of 164 patients (79.9%). Thoracotomy was required in 32 patients (19.5%) and subxiphoid patch in 1 patient (0.6%). Over a mean of 12.9 months (range 1-62 months), 3 patients (1.8%) required revision of the rate sensing lead/coil or superior vena cava coil after development of lead compression fractures in the region of the clavicle and first rib. In all 3 patients the leads had been implanted via subclavian puncture (2.6% of patients in whom the subclavian technique was utilized). Two patients presented with spurious shocks. One patient was asymptomatic. CONCLUSIONS: When venous access is obtained via subclavian puncture, subclavian crush syndrome may develop in patients with transvenous defibrillator systems. Patients may be asymptomatic and lead fractures may go unrecognized. When implanting transvenous defibrillator systems, strong consideration should be given to obtaining venous access primarily via the cephalic cut-down technique.

Aged↗

The technique and safety of transseptal left heart catheterization: the Massachusetts General Hospital experience with 1,279 procedures.

With the introduction of interventional procedures such as percutaneous mitral valvuloplasty and radiofrequency ablation of left-sided bypass tracts, there has been renewed interest in the technique of transseptal left heart catheterization. We review our experience with 1,279 transseptal catheterizations performed over the last 10 years. The most common indications for transseptal catheterization included direct measurement of left atrial pressure or access to the left ventricle in patients with prosthetic aortic or mitral valves, and in patients undergoing percutaneous mitral valvuloplasty. A total of 17 major complications occurred (1.3%), including cardiac tamponade (15 patients, 1.2%), systemic emboli (1 patient, 0.08%), and death secondary to aortic perforation (0.08%). We conclude that when performed by experienced operators, transseptal left heart catheterization is associated with low morbidity and mortality.

Adolescent↗

Analysis of the initiation of spontaneous monomorphic ventricular tachycardia by stored intracardiac electrograms.

OBJECTIVES: This study was designed to analyze stored intracardiac electrograms generated during spontaneous monomorphic ventricular tachycardia to examine the possible mechanisms responsible for the initiation of ventricular tachycardia in a group of postinfarction patients. BACKGROUND: Implantable cardioverter-defibrillators capable of storing electrograms during an arrhythmic event provide an intracardiac electrogram analog to Holter ambulatory electrocardiographic monitoring. Such electrograms are of value in arrhythmia diagnosis and in determining the appropriateness of implantable cardioverter-defibrillator therapy and may aid in understanding the initiation of ventricular arrhythmias. METHODS: We studied 73 stored electrograms in 22 postinfarction patients with spontaneous monomorphic ventricular tachycardia. Premature depolarizations before tachycardia were classified by morphology and number. Electrogram morphology was compared with the morphology of the baseline rhythm and ventricular tachycardia. Prematurity was assessed by the coupling interval and a calculated prematurity ratio. RESULTS: During baseline rhythm, ectopic activity was present in 30 (41%) of 73 stored episodes. Ventricular tachycardia was preceded by a short-long-short sequence in 14% of episodes and by a rapid ventricular rhythm in 5.5% of episodes. The onset of ventricular tachycardia was marked by single premature depolarizations in 33 episodes (45%), by pairs in 16 (22%) and by multiple complexes in 24 (33%). Morphology was similar to that of the ensuing tachycardia in 35 episodes (48%). The mean coupling interval was 364 ms, and the mean prematurity ratio was 0.56. In all 10 episodes (14%) where the prematurity ratio was < 0.40, a short-long-short sequence was responsible. When classified by morphology, the mean prematurity ratio of depolarizations dissimilar to ventricular tachycardia (0.53) was significantly less than that of the morphologically similar group (0.60, p = 0.035). CONCLUSIONS: In this select group of postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter-defibrillators, ventricular tachycardia was most often preceded by late-coupled premature depolarizations. Not infrequently, a short-long-short sequence occurred before tachycardia. Premature depolarizations with a morphology different from that of the tachycardia occurred earlier in the cardiac cycle than did those with a morphology similar to that of the tachycardia. These findings may reflect different mechanisms of ventricular tachycardia initiation.

Adolescent↗

Submammary pacemaker implantation: a unique tunneling technique.

Submammary pacemaker implantation offers women a cosmetically acceptable alternative to the standard pectoral implant. We present a novel method of submammary implantation performed on ten women aged 13-54 years. The lead electrodes are tunneled from the infraclavicular to the inframammary incision using a long needle, guidewire, and introducers/dilators in a manner analogous to the retained guidewire technique used for standard lead insertion. The procedure can generally be performed under local anesthesia. All patients tolerated the procedure well without acute complications. Over 2- to 23-month follow-up, there were no lead dislodgments. No patients developed mastitis or incisional complications, and all have been extremely satisfied with the cosmetic results. With proper technique, submammary pacemaker implantation can be performed under local anesthesia with minimal patient discomfort and optimal cosmesis.

Adolescent↗

A comparison of VVIR and DDDR pacing following cardiac transplantation.

UNLABELLED: We compared the clinical course of patients paced in VVIR versus DDDR mode to determine the most appropriate method of pacing following cardiac transplantation. Pacemaker implantation was required in 9 of 90 orthotopic cardiac transplants (10%). Indications included sinus bradycardia or sinus arrest (8 patients) and AV node dysfunction (1 patient). VVIR pacemakers were implanted in four patients and DDDR in five patients. DDDR patients: The mean P wave was 1.7 mV and the mean atrial stimulation threshold was 0.8 V (at 0.5 msec). During follow-up of 20 months, two atrial lead complications developed (29% of leads in 33% of patients). No lead complications were directly related to endomyocardial biopsy. VVIR patients: All four patients developed VA conduction with mean VA time 180 msec (160-240 msec). Two patients developed pacemaker syndrome. CONCLUSIONS: VA conduction and pacemaker syndrome may develop in cardiac transplant recipients paced in the VVIR mode. Dual chamber pacing is technically feasible and preferable following cardiac transplantation.

Adult↗

Multinucleated cells elicited in response to implants of devitalized bone particles possess receptors for calcitonin.

The introduction into soft tissues of particulate materials resistant to digestion results in the induction of a "foreign-body giant-cell reaction." We have examined the relation between osteoclasts and foreign-body giant cells by comparing the tissue responses elicited by subcutaneous implants of devitalized, mineral-containing bone particles (BP), nonresorbable plastics such as polymethylmethacrylate (PMMA), or both. Implantation of BP results in the recruitment of multinucleated cells with features of in osso osteoclasts including tartrate-resistant acid phosphatase activity, contact-mediated resorption of BP, membrane specializations (ruffled borders and clear zones), and inhibition of resorption by calcitonin treatment of animals. In the present study, an autoradiographic technique employing 125I-salmon calcitonin was used to demonstrate the presence of receptors for this hormone on multinucleated cells from BP implants. In contrast, outgrowth cells from PMMA implants lacked calcitonin receptors. Demonstration of features of the osteoclastic phenotype in multinucleated cells elicited in response to BP supports the hypothesis that the mineralized matrix of bone may be a requirement for acquisition of the osteoclast phenotype.

Animals↗

Conjunctivitis, tracheitis, and pneumonia associated with herpesvirus infection in green sea turtles.

Fourteen juvenile (15- to 20-month-old) green sea turtles (Chelonia mydas), representative of a group of sea turtles with clinical signs of respiratory tract disease, were euthanatized and submitted for necropsy. Macroscopically, lesions included periglottal necrosis, tracheitis with intraluminal caseous and laminated necrotic debris, and severe pneumonia. Several turtles had caseous conjunctival exudate covering the eyes. Microscopically, the turtles had fibrinonecrotic inflammation around the glottal opening, tracheitis, and severe bronchopneumonia and interstitial pneumonia. In multifocal areas, periglottal and tracheal epithelial cells adjacent to areas of necrosis had hypertrophic nuclei with amphophilic intranuclear inclusions. A mixed population of primarily gram-negative microorganisms was isolated from the tracheal and glottal lesions. Attempts at viral isolation in cultures of green sea turtle kidney cells resulted in the development of cytopathic effects characterized by giant cell formation and development of intranuclear inclusions. Using electron microscopy, intranuclear viral particles (88 to 99 nm in diameter) were seen in inclusion-containing tracheal and glottal epithelial cells and infected green sea turtle kidney cells; particles were consistently seen enveloping from nuclear membranes, and mature particles (132 to 147 nm) were found in the cytoplasm. On the basis of size, conformation, location, and presence of an envelope, the particles most closely resembled those of herpes-viruses.

Animals↗

Chronic encephalomyelitis caused by canine distemper virus in a Bengal tiger.

A chronic progressive neurologic disease was observed and monitored for 18 months in a young, tamed Bengal tiger. Clinical, serologic, and neuropathologic evidence of canine distemper virus infection was seen. Clinical signs included convulsions, myoclonus, and slowly progressive ataxia. Marked increases in neutralizing antibodies against canine distemper virus were seen in the serum and cerebrospinal fluid. Neuropathologic findings were nonsuppurative meningoencephalomyelitis, with perivascular cuffing, demyelination, and inclusion bodies typical of canine distemper virus. It was concluded that, in light of this case and an earlier report of canine distemper in lion cubs, vaccination of this subgroup of carnivores with a killed vaccine may be beneficial if exposure to other animals susceptible to canine distemper is anticipated.

Animals↗

Rheumatoid synovial cell morphologic changes induced by a mononuclear cell factor in culture.

Adherent rheumatoid synovial cells in culture produce large amounts of prostaglandin E2 (PGE2) and collagenase. When exposed to a monocyte-derived factor, such cells exhibit marked increases in PGE2 and collagenase production. In addition, cellular morphology becomes more stellate. In the presence of this factor, indomethacin inhibits both PGE2 production and the stellate changes, whereas collagenase production usually continues at a high rate. Addition of PGE2 to cultures reproduces the stellate change as does the cyclic adenosine monophosphate (cAMP) analog 8-bromo-cAMP. Colchicine inhibits morphologic transformation induced by the monocyte-derived factor, whereas cytochalasin B has no effect. It appears that the stellate morphology is dependent upon PGE2-induced cAMP stimulation and is not related to collagenase production per se.

8-Bromo Cyclic Adenosine Monophosphate↗

Self-associating IgG rheumatoid factors stimulate monocytes to release prostaglandins and mononuclear cell factor that stimulates collagenase and prostaglandin production by synovial cells.

Self-associating IgG rheumatoid factors isolated from three patients with rheumatoid arthritis activated human monocytes to release prostaglandin E2 as well as a previously described mononuclear cell factor, which stimulates human synovial cells to release additional prostaglandin E2 and collagenase. Thus, the immune complexes composed of self-associating IgG rheumatoid factors can contribute to the processes that destroy cartilage and bone in patients with rheumatoid arthritis.

Humans↗

The synovial-like membrane at the bone-cement interface in loose total hip replacements and its proposed role in bone lysis.

UNLABELLED: The membrane present at the bone-cement interface was retrieved from twenty patients with a loose, non-septic failed total hip replacement at a site clearly remote from the pseudocapsule that reformed postoperatively. The orientation of the membrane was carefully marked to identify the surface in contact with cement. The membrane was studied histologically, histochemically, by cell culture, by organ culture, and by assessment of its ability to synthesize prostaglandin E2 and collagenase. This membrane, rather than being a nondescript so-called fibrous membrane, has the histological and histochemical characteristics of a synovial-like lining. The synovial-like cells are adjacent to the cement layer. Deep to them macrophages predominate. Inflammatory cells are absent. Cell cultures of this membrane contain stellate cells similar to those found in cell cultures of normal and rheumatoid synovial tissue. This membrane has the capacity to produce large amounts of prostaglandin E2 and collagenase. CLINICAL RELEVANCE: This transformation of tissue at the bone-cement interface in patients with a non-septic, loose total hip component to a synovial-like tissue with the capacity to generate prostaglandin E2 and collagenase may explain the progressive lysis of bone that is seen in some patients with loose cemented total joint implants. Loosening of the component may be a stimulus to the synthetic activity of this tissue, which leads to further resorption of bone. Understanding and the possibility of pharmacological control of this membrane may contribute to improved duration of total joint implants.

Bone Resorption↗

Glucoprivic feeding behavior in absence of other signs of glucoprivation.

When rats were denied immediate access to food after subcutaneous injection of 2-deoxy-D-glucose (2DG), the glucoprivically induced sympathoadrenal hyperglycemia subsided spontaneously within 6 h. However, if food was returned to the rats 6 h after 2DG injection, they still ate significantly more than after saline control injections. Rats injected with insulin also increased their feeding even when food was withheld until the animals had returned to normoglycemia. Injections of exogenous glucose sufficient to elevate blood glucose concentrations above normal failed to inhibit increased feeding observed when food was returned 6 h after injection of regular insulin. These data show that 2DG and insulin-induced feeding can occur in the absence of overt signs of glucoprivation and suggest that the glucoprivic control may be operable in the day-to-day control of feeding when other signs of glucoprivation are not readily observable.

Animals↗