Search

Transvenous lead extraction (TLE) has evolved as one of the most crucial treatment options for patients with cardiac device-related systemic infection (CDRSI).The aim of this study was to characterize the procedural outcome and risk factors of patients with CDRSI undergoing TLE.A subgroup analysis of patients with CDRSI of the GALLERY (GermAn Laser Lead Extraction RegistrY) database was performed. Predictors for complications, procedural failure, and all-cause mortality were evaluated.A total of 722 patients (28.6%) in the GALLERY had "systemic infection" as extraction indication. Patients with CDRSI were older (70.1 ± 12.2 years vs 67.3 ± 14.3 years; P.001) and had more comorbidities than patients with local infections or noninfectious extraction indications. There were no differences in complete procedural success (90.6% vs 91.7%; P = .328) or major complications (2.5% vs 1.9%; P = .416) but increased procedure-related (1.4% vs 0.3%; P = .003) and all-cause in-hospital mortality (11.1% vs 0.6%; P.001) for patients with CDRSI. Multivariate analyses revealed lead age ≥10 years as a predictor for procedural complications (odds ratio [OR] 3.23; 95% confidence interval [CI] 1.58-6.60; P = .001). Lead age ≥10 years (OR 2.57; 95% CI 1.03-6.46; P = .04) was also a predictor for procedural failure. We identified left ventricular ejection fraction30% (OR 1.70; 95% CI 1.00-2.99; P = .049), age ≥75 years (OR 2.1; 95% CI 1.27-3.48; P = .004), chronic kidney disease (OR 1.92; 95% CI 1.17-3.14; P = .01), and overall procedural complications (OR 5.15; 95% CI 2.44-10.84; P.001) as predictors for all-cause mortality.Patients with CDRSI undergoing TLE demonstrate an increased rate of all-cause in-hospital, as well as procedure-related mortality, despite having comparable procedural success rates. Given these data, it seems paramount to develop preventive strategies to detect and treat CDRSI in its earliest stages.

We evaluated the performance of implantable loop recorders (ILRs) with different detection algorithms and looked for artifacts and therapeutic consequences and their dependence on patient factors.586 RevealLinq™ ILRs (first generation (NT): n = 335; second generation with TruRhythm™ (TR): n = 251) were implanted during 2014-2021 (syncope n = 206; embolic stroke of unknown source (ESUS) n = 380). Automatically detected EGM episodes (n = 18,650) were classified as correct or incorrect for asystole (AS), atrial fibrillation (AF) or tachycardia (TA). Incorrect episodes were caused by loss of signal (LO), noise (NO), extrasystole (ES) and T-wave oversensing (TWO). Left directed R axes, lower R-amplitudes and older age were related to artifacts. Results were separated by indication. In ESUS patients TR reduced total median artifact episodes: 0.6 (0-7) vs 0 (0-5) (p0.03) and median artifact examination time: 0.3 (0-3.5) vs 0 (0-2.5) (p = 0.03) per patient-year. This benefit is caused by significant reductions in total AS and ES-AS artifacts. The total positive predictive value (PPV) improved only in syncope patients (45 vs 71%, p = 0.002). Accordingly in syncope patients with TR more therapeutic consequences could be established (log rank 0.003).Patients R-axis and measured R-amplitudes during implantation predicted artifacts. This should be taken into account during ILR implantation. Total artifacts, AS artifacts and time spent for artifact analysis was reduced by the new TR detection algorithm in ESUS patients, whereas total artifacts remained unchanged in syncope patients despite reduction of AS artifacts. However TR had no effect on AF and TA episode detection and therefore has to be improved.

Background Patients with atrial fibrillation (AF) often have sleep apnea (SA), but diagnosis of SA with polysomnography is costly. SA monitoring is a pacemaker feature that measures respiratory disturbance index, the sum of abnormal respiratory events divided by sleep duration. Objective The purpose of this study was to evaluate the incidence and severity of SA and its association with AF in an unselected population fitted with pacemakers. Methods RESPIRE (REgistry of Sleep APnea monItoring and Atrial Fibrillation in pacemakeR patients) was a multicenter, international, observational, open-label study following adult subjects for 18 months after implantation with an SA monitoring–enabled dual-chamber pacemaker. Severe SA was defined as average respiratory disturbance index ≥20 from implantation to follow-up visit. The first co-primary end point was the difference in significant AF (cumulative AF episodes lasting ≥24 hours over 2 consecutive days) between subjects with severe and those nonsevere SA at 12 months in the full analysis set (N = 553). The second co-primary end point was the rate of major serious adverse events at 18 months in the modified intention-to-treat set (N = 1024). Results Severe SA was detected in 31.1% (172 of 553). A higher incidence of significant AF was reported in patients with severe SA than in patients with nonsevere SA (25.0% vs 13.9%; difference 11.1%; 95% confidence interval 3.7%–18.4%; P = .002). Significant AF increased with time in both groups, but at a faster rate in the severe SA group. No intergroup difference in the overall rate of major serious adverse events was observed (P = .065). Conclusion SA screening over 12 months identified severe SA in almost one-third of unselected patients fitted with pacemakers. Severe SA was associated with a higher incidence of significant AF.

Sensing of left ventricular (LV) activity in some devices used for cardiac resynchronization therapy (CRT) was designed primarily to prevent the delivery of an LV stimulus into the LV vulnerable period. Such a sensing function of the LV channel is not universally available in contemporary CRT devices. Recordings of LV electrograms may provide special diagnostic data unavailable solely from the standard right ventricular electrogram and corresponding marker channel. We used the LV sensing function of Biotronik CRT defibrillators to find 3 cases of dissimilar ventricular rhythms or tachyarrhythmias. Such arrhythmias are potentially important because concomitant slower right ventricular activity may prevent or delay implantable cardioverter-defibrillator therapy for a life-threatening situation involving a faster and more serious LV tachyarrhythmia. Dissimilar ventricular rhythms may not be rare and may account for cases of unexplained sudden death with a normally functioning implantable cardioverter-defibrillator and no recorded terminal arrhythmia.

Background: Because the risk of developing malignant tumors after heart transplantation is approximately 100-fold higher, methods for rapid diagnosis must be developed to allow early and aggressive treatment in these patients. Although tumor markers have been used frequently for surveying already detected cancer, we studied their value in screening for tumors in heart transplant patients. Methods The levels of the tumor markers CEA, CA19-9, CA125, CA72-4, TPA, TPS, and CYFRA 21-1 were determined prospectively in 3-month intervals in 91 heart transplant patients between 1993 and 1998. Results In eight patients a definite diagnosis of cancer was made during the marker survey (mean observation time 2.85 ± 1.3 years), including bronchogenic carcinoma in six, renal carcinoma in one, and colon cancer in one. All patients with bronchogenic carcinoma were smokers. The markers had a sensitivity below 60% to detect cancer. Given a 2-fold cutoff level (10 ng/mL), the CEA was the only marker with sufficient specificity (93.8%, only one false-positive result). Two patients were symptom-free even though they had elevated CEA levels. In one of those patients, disseminated intractable cancer was diagnosed at first evaluation, whereas no tumor was found in the other case at first evaluation. Subsequently, by means of fluorodeoxyglucose positron emission tomography, a hypermetabolic region was found in the right upper mediastinum. Control computed tomographic scan 4 weeks after the first investigation showed disseminated intractable disease also in this patient. Another heart transplant patient with colon cancer showed a normalization of the CEA after hemicolectomy and an increase in the CEA when liver dissemination developed. There was a relationship between cardiac death and CA125 and TPS in some heart transplant patients. Conclusions We conclude that the CEA is the only tumor marker with adequate sensitivity and specificity to detect subclinical malignancies in the follow-up of heart transplant patients. However, because of several limitations (limited diagnostic and therapeutic possibilities and enormous costs), we cannot recommend screening by tumor markers on a regular basis. Because of the elevated risk of cancer in patients who had organ transplantation, further prophylactic measures, especially smoking cessation programs, must be developed. Once a malignancy is diagnosed, tumor markers can help target clinical decisions. Additionally, nonspecific increases in CA125 and TPS levels might be related to nonmalignant circulatory disturbances and cardiac death.

CA 125, known as a marker for ovarian cancer with hypothetical but hitherto uncharacterized biologic functions, was reported to be elevated in some not-well-defined benign conditions. There are no reports on fluctuations of CA 125 related to cardiac function, especially the failing heart and neurohumoral factors such as norepinephrine or atrial natriuretic peptid/e.CA 125 blood levels were determined in patients with heart failure before and after heart transplantation (HTx). In 71 patients, parallel determinations of norepinephrine, atrial natriuretic peptide, pulmonary capillary wedge pressure, and right atrial filling pressure were done. CA 125 levels also were prospectively studied in patients with heart failure with stabilization (n = 25) or worsening of the clinical status (n = 9) and after HTx (n = 25). Parallel determinations of the tumor markers CEA, CA 199, CA 153, TPS, and TPA were also done. The results were grouped according to the clinical status (New York Heart Association class) of the patients. CA 125 was significantly correlated with neurohormones and filling pressures. Follow-up investigations revealed a decrease of CA 125 levels after HTx (401 +/- 259 U/L vs 33 +/- 22 U/L, P.001, n = 25) or stabilization (429 +/- 188 U/L vs 78 +/- 35 U/L, P.001, n = 25) and an increase during worsening of heart failure (42 +/- 25 U/L vs 89 +/- 32 U/L, P.01, n = 9). In 4 patients after HTx, unexpected death was preceded by rising CA 125 levels. CEA, CA 199, CA 153, TPS, or TPA did not correlate with heart failure status or clinical events.CA 125 is a marker of the clinical and hemodynamic status and the course of patients with heart failure before and after heart transplantation. The determination of CA 125 serum levels may be an additional tool in the management of these patients. In patients with cancer, these "nonspecific" changes must be considered when CA 125 levels are determined. Whether CA 125 has a specific biologic role in heart failure deserves further studies.

Background : Because of donor shortage, heart transplantation (HTx) as therapy for end-stage heart failure is limited by a mortality rate of 25% on waiting lists, and lists are steadily increasing. Aim : To analyse whether an intensive medical therapeutic regimen for heart failure (based on the results of frequent haemodynamic studies) can delay or even prevent the need for HTx. Methods : Data analysis of 517 patients who were referred to our institution for HTx from 1984 to 1996 is presented. Characteristics and management of 359 non-emergency, New York Heart Association (NYHA) III or IV heart transplant candidates, without contraindications (and with sufficient compliance) are described. All candidates receiving conventional therapy with ACE inhibitors, digitalis and diuretics at entry were evaluated. Drug therapy was intensified as follows: a further reduction of preload; a further reduction of afterload; individualised diuresis; and amiodarone therapy. Results : Under this regimen, clinical and haemodynamic parameters improved in many patients. Only 95 patients (26%) were primary non-responders to intensified medical therapy and had to be listed for HTx early (during the first year of follow-up). Actuarial survival rates of the early listed versus the early responding HTx candidates, at 1 and 5 years, were 68.3%/87% and 41%/59%, respectively (p=0.02). An additional benefit of co-therapy with amiodarone and calcium antagonists was found. The most important mode of cardiac death was sudden (32% at 5 years), whereas mortality due to pump failure was much lower (13% at 5 years). Only 38 patients (16%):had to be listed for HTx in further follow-up. Conclusions : Intensive medical therapy in heart transplant candidates may be an alternative to immediate HTx, especially in times of donor shortage or in countries without a transplantation program. Responders to therapy showed a similar or even better prognosis than HTx patients. This conservative approach may allow available donor hearts to be saved for those patients most needing a transplant.

There is good epidemiologic evidence that hypertension is associated with a high risk of cardiovascular disease. However, primary intervention trials have failed to demonstrate that a reduction in blood pressure in hypertensive patients reduces morbidity and mortality from cardiac events. Since various antihypertensive drugs adversely affect lipoprotein metabolism, these drugs may increase associated coronary risk and offset the beneficial effects of lowering blood pressure. This article reviews the effects of various antihypertensive drugs on plasma lipids, lipoproteins, and apolipoproteins. They can be summarized as follows: thiazide-type diuretics cause a marked elevation of plasma triglycerides and very low-density lipoprotein (VLDL) and minor increases in total cholesterol and low-density lipoprotein (LDL), but have little effects on high-density lipoprotein (HDL). The nonselective beta-blockers do not significantly affect total cholesterol and LDL, but increase total triglycerides and VLDL and decrease HDL. The changes in plasma lipids and lipoproteins caused by cardioselective beta-blockers and beta-blockers with intrinsic sympathomimetic activity are qualitatively similar but less pronounced. Calcium antagonists and angiotensin-converting enzyme inhibitors appear to have no significant effects on plasma lipids. alpha 1-Inhibitors reduce total triglycerides, total cholesterol, VLDL, and LDL and increase HDL. The possible mechanisms by which antihypertensive drugs affect cellular lipid metabolism (e.g., LDL receptor, lipid synthesis, lipoprotein lipase, lecithin cholesteryl acyltransferase, acylcholesteryl acyltransferase, and cholesteryl ester hydrolase) are described. The clinical significance of changes in blood lipids and cellular lipid metabolism caused by antihypertensive drugs is not yet totally clear. Nevertheless, before antihypertensive drug treatment is initiated, blood lipid levels should be measured to identify preexisting hyperlipidemia.(ABSTRACT TRUNCATED AT 250 WORDS)