Incidence of carditis and predictors of pacemaker implantation in patients hospitalized with Lyme disease

Background Lyme carditis, defined as direct infection of cardiac tissue by Borrelia bacteria, affects up to 10% of patients with Lyme disease. The most frequently reported clinical manifestation of Lyme carditis is cardiac conduction system disease. The goal of this study was to identify the incidence and predictors of permanent pacemaker implantation in patients hospitalized with Lyme disease. Methods A retrospective cohort analysis of the Nationwide Inpatient sample was performed to identify patients hospitalized with Lyme disease in the US between 2003 and 2014. Patients with Lyme carditis were defined as those hospitalized with Lyme disease who also had cardiac conduction disease, acute myocarditis, or acute pericarditis. Patients who already had pacemaker implants at the time of hospitalization (N = 310) were excluded from the Lyme carditis subgroup. The primary study outcome was permanent pacemaker implantation. Secondary outcomes included temporary cardiac pacing, permanent pacemaker implant, and in-hospital mortality. Results Of the 96,140 patients hospitalized with Lyme disease during the study period, 10,465 (11%) presented with Lyme carditis. Cardiac conduction system disease was present in 9,729 (93%) of patients with Lyme carditis. Permanent pacemaker implantation was performed in 1,033 patients (1% of all Lyme hospitalizations and 11% of patients with Lyme carditis-associated conduction system disease). Predictors of permanent pacemaker implantation included older age (OR: 1.06 per 1 year; 95% CI:1.05–1.07; P<0.001), complete heart block (OR: 21.5; 95% CI: 12.9–35.7; P<0.001), and sinoatrial node dysfunction (OR: 16.8; 95% CI: 8.7–32.6; P<0.001). In-hospital mortality rate was higher in patients with Lyme carditis (1.5%) than in patients without Lyme carditis (0.5%). Conclusions Approximately 11% of patients hospitalized with Lyme disease present with carditis, primarily in the form of cardiac conduction system disease. In this 12-year study, 1% of all hospitalized patients and 11% of those with Lyme-associated cardiac conduction system disease underwent permanent pacemaker implantation.

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A novel lamin A/C mutation in a family with dilated cardiomyopathy, prominent conduction system disease, and need for permanent pacemaker implantation

American Heart Journal ◽

10.1067/mhj.2002.126737 ◽

2002 ◽

Vol 144 (6) ◽

pp. 1081-1086 ◽

Cited By ~ 47

Author(s):

Ray E. Hershberger ◽

Emily L. Hanson ◽

Petra M. Jakobs ◽

Hugh Keegan ◽

Kelly Coates ◽

...

Keyword(s):

Dilated Cardiomyopathy ◽

Pacemaker Implantation ◽

Permanent Pacemaker ◽

Conduction System ◽

Lamin A ◽

Permanent Pacemaker Implantation ◽

System Disease ◽

Conduction System Disease

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Sodium channel kinetic changes that produce Brugada syndrome or progressive cardiac conduction system disease

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01025.2005 ◽

2007 ◽

Vol 292 (1) ◽

pp. H399-H407 ◽

Cited By ~ 33

Author(s):

Zhu-Shan Zhang ◽

Joseph Tranquillo ◽

Valentina Neplioueva ◽

Nenad Bursac ◽

Augustus O. Grant

Keyword(s):

Action Potential ◽

Sodium Channel ◽

Brugada Syndrome ◽

Sodium Current ◽

Conduction System ◽

Cardiac Conduction ◽

Cardiac Conduction System ◽

Wild Type ◽

System Disease ◽

Conduction System Disease

Some mutations of the sodium channel gene NaV1.5 are multifunctional, causing combinations of LQTS, Brugada syndrome and progressive cardiac conduction system disease (PCCD). The combination of Brugada syndrome and PCCD is uncommon, although they both result from a reduction in the sodium current. We hypothesize that slow conduction is sufficient to cause S-T segment elevation and undertook a combined experimental and theoretical study to determine whether conduction slowing alone can produce the Brugada phenotype. Deletion of lysine 1479 in one of two positively charged clusters in the III/IV inter-domain linker causes both syndromes. We have examined the functional effects of this mutation using heterologous expression of the wild-type and mutant sodium channel in HEK-293-EBNA cells. We show that ΔK1479 shifts the potential of half-activation, V1/2m, to more positive potentials ( V1/2m = −36.8 ± 0.8 and −24.5 ± 1.3 mV for the wild-type and ΔK1479 mutant respectively, n = 11, 10). The depolarizing shift increases the extent of depolarization required for activation. The potential of half-inactivation, V1/2h, is also shifted to more positive potentials ( V1/2h = −85 ± 1.1 and −79.4 ± 1.2 mV for wild-type and ΔK1479 mutant respectively), increasing the fraction of channels available for activation. These shifts are quantitatively the same as a mutation that produces PCCD only, G514C. We incorporated experimentally derived parameters into a model of the cardiac action potential and its propagation in a one dimensional cable (simulating endo-, mid-myocardial and epicardial regions). The simulations show that action potential and ECG changes consistent with Brugada syndrome may result from conduction slowing alone; marked repolarization heterogeneity is not required. The findings also suggest how Brugada syndrome and PCCD which both result from loss of sodium channel function are sometimes present alone and at other times in combination.

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