Yield and consistency of arrhythmia detection with patch electrocardiographic monitoring: The Multi-Ethnic Study of Atherosclerosis.

BACKGROUND: Patch electrocardiographic (ECG) monitors permit extended noninvasive ambulatory monitoring. To guide use of these devices, information is needed about their performance. We sought to determine in a large general population sample the acceptability of patch ECG monitors, the yield of arrhythmia detection, and the consistency of findings in participants monitored twice. METHODS: In the Multi-Ethnic Study of Atherosclerosis, 1122 participants completed one or two monitoring episodes using the Zio Patch XT, a single-channel ECG patch monitor capable of recording for 14 days. Recordings were analyzed for atrial fibrillation (AF), atrial flutter, atrioventricular block, pauses, and supraventricular and ventricular ectopy. RESULTS: The mean(SD) age at the time of monitoring was 75(8) years, 52% were men, and 15% had a prior history of clinically-recognized AF/flutter. The median monitoring duration was 13.8 days. Among 804 participants with no prior clinical history of AF/flutter and at least 12 days of monitoring on a single device, AF/flutter was detected in 32 (4.0%); in 38% of these, AF/flutter was first detected during days 3 through 12 of monitoring. In participants monitored twice, findings from the two devices showed excellent agreement for supraventricular and ventricular ectopic beats per hour, but only fair agreement for high-grade atrioventricular block and pauses of >3 s duration. CONCLUSIONS: In a general population of older individuals, new diagnoses of AF/flutter were made in 4.0% of participants without a prior history. A single monitoring episode accurately estimated rates of supraventricular and ventricular ectopy.

Evidence for reduced susceptibility to cardiac bradycardias in South Asians compared with Caucasians.

OBJECTIVES: To investigate ethnic differences in susceptibility to bradycardias in South Asian and white European patients in the UK by determining rates of permanent pacemaker (PPM) implantation for sinus node dysfunction (SND) and atrioventricular block (AVB) in each ethnic group. METHODS: We carried out a retrospective cohort study into new PPM implantation during the period from 1 May 2006 to 31 March 2014, in patients of South Asian and Caucasian ethnicity resident in Leicestershire, UK. Numbers of individuals at risk in each ethnic group were derived from UK National Census data of 2011. Crude, and age-standardised incidence rates and risk ratios per 1000 population of PPM implantation were calculated for Caucasians and South Asians. RESULTS: During the study period, 4883 individuals from the Leicestershire population of 980 328 underwent PPM implantation, a cumulative implantation rate of 4.98/1000 population. The population cumulative PPM implantation rate for SND was 1.74/1000, AVB 2.83/1000 and other indications 0.38/1000 population. The crude incidence in Caucasians (6.15/1000 population) was higher than in South Asians (1.07/1000 population) and remained higher after age standardisation (5.60/1000 vs 2.03/1000, P<0.001). The age-standardised cumulative PPM implantation rates were lower in South Asians for both SND (0.53/1000 in South Asians; 1.97/1000 in Caucasians, P<0.001) and AVB (1.30/1000 in South Asians; 3.17/1000 in Caucasians, P<0.001). Standardised risk ratios (95% CI) for PPM implantation in South Asians compared with Caucasians for all pacing indications, SND and AVB were 0.36 (95% CI 0.36 to 0.37), 0.27 (95% CI 0.27 to 0.28) and 0.41 (95% CI 0.41 to 0.42), respectively. CONCLUSIONS: Rates of PPM implantation are lower in South Asians residing in the UK, compared with Caucasians. This observation raises the possibility of lower inherent susceptibility to bradycardias in South Asians compared with Caucasians. Studies aimed at identifying underlying mechanisms, including possible genetic differences, are warranted.

Fibrosis and coronary perfusion - a cardiovascular disease risk in an African male cohort: The SABPA study.

Low-grade inflammation has been correlated with risk factors of cardiovascular diseases (CVD). Whether the pro-inflammatory and thrombotic ratio (fibrosis) may contribute to CVD is not known. We therefore aimed to assess whether Cornell Product left ventricular hypertrophy (LVH) is associated with fibrosis and coronary perfusion (silent ischemia) in a bi-ethnic male cohort from South Africa. A cross sectional study was conducted including 165 African and Caucasian men between the ages of 20-65. Fasting blood samples were obtained to measure fibrinogen, C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α). Ambulatory blood pressure, ECG and 12 lead ECG measures were obtained to determine silent ischemic events (ST events) and LVH, respectively. Africans revealed more silent ischemia, higher 24 h blood pressure, inflammatory, coagulation as well as fibrosis levels than Caucasians. In a low-grade inflammatory state (CRP > 3 mg/l), Africans revealed higher fibrosis (p ≤ 0.01) values, but lower IL-6 and TNF-α values than Caucasians. Linear regression analyses in several models demonstrated positive associations between silent ischemia and fibrosis [Adj. R(2) 0.23; ß 0.35 (95% CI 0.13, 0.58), p ≤ 0.01]. In a low-grade inflammatory state (CRP>3mg/l), fibrinogen predicted AV-block in African men [OR 3.38 (95% CI 2.24, 4.53); p = 0.04]. Low-grade inflammation may induce AV-block through mechanisms involving fibrosis and ischemia to increase the burden on the heart in African men.

Chagas disease: don't forget it in Latin American patients with heart block!

Chagas disease is caused by the parasite Trypanosoma cruzi, and mostly affects poor rural populations of central and south America. It is mainly acquired by bugs (triatoma) but also by ingestion of the parasite (fresh fruit juices) or by foetal-maternal blood passing. Despite an important decrease in transmission during the last decades in several countries, millions of patients are still chronically infected and most of them are asymptomatic. In 2012-2013, two cases were admitted in our cardiac intensive care unit (ICU) with heart block due to Chagas cardiomyopathy. Diagnosis was established by echocardiography and positive serological results for Trypanosoma cruzi. This report underlines that in cases of heart failure and conduction abnormalities of unclear aetiology, Chagas disease should be taken into consideration, even in patients originating from non-endemic countries.

Mutational spectrum in the Ca(2+)--activated cation channel gene TRPM4 in patients with cardiac conductance disturbances.

Very recently, mutations in the TRPM4 gene have been identified in four pedigrees as the cause of an autosomal dominant form of cardiac conduction disease. To determine the role of TRPM4 gene variations, the relative frequency of TRPM4 mutations and associated phenotypes was assessed in a cohort of 160 unrelated patients with various types of inherited cardiac arrhythmic syndromes. In eight probands with atrioventricular block or right bundle branch block--five familial cases and three sporadic cases--a total of six novel and two published TRPM4 mutations were identified. In patients with sinus node dysfunction, Brugada syndrome, or long-QT syndrome, no mutations were found. The novel mutations include six amino acid substitutions and appeared randomly distributed through predicted TRPM4 protein. In addition, eight polymorphic sites including two in-frame deletions were found. Mutations separated from polymorphisms by absence in control individuals and familial cosegregation in some families. In summary, TRPM4 gene mutations appear to play a major role in cardiac conduction disease but not for other related syndromes so far. The phenotypes are variable and clearly suggestive of additional factors modulating the disease phenotype in some patients.

Molecular and clinical characterization of a novel SCN5A mutation associated with atrioventricular block and dilated cardiomyopathy.

BACKGROUND: Increased susceptibility to dilated cardiomyopathy has been observed in patients carrying mutations in the SCN5A gene, but the underlying mechanism remains unclear. In this study, we identified and characterized, both in vitro and clinically, an SCN5A mutation associated with familial progressive atrioventricular block of adult onset and dilated cardiomyopathy in a Chinese family. METHODS AND RESULTS: Among 32 family members, 5 were initially diagnosed with atrioventricular block after age 30; 4 were studied, 3 of whom later developed dilated cardiomyopathy. We found a heterozygous single-nucleotide mutation resulting in an amino acid substitution (A1180V) in all studied patients and in 6 other younger unaffected members but not in 200 control chromosomes. When expressed with the beta1 subunit, the mutated channels exhibited a -4.5-mV shift of inactivation with slower recovery leading to a rate-dependent Na(+) current reduction and a moderate increase in late Na(+) current. Clinical study revealed that although QRS duration decreased with increasing heart rate in noncarrier family members, this change was blunted in unaffected carriers whose ECG and heart function were normal. Resting corrected QT interval of unaffected carriers was significantly longer than that of noncarriers, even though it was still within the normal range. CONCLUSIONS: A1180V expresses a mild Na(+) channel phenotype in vitro and a corresponding clinical phenotype in unaffected mutation carriers, implying that A1180V caused structural heart disease in affected carriers by disturbing Na(+) influx and, hence, cellular Na(+) homeostasis. The high penetrance of A1180V suggests this phenotype as a high risk factor for dilated cardiomyopathy with preceding atrioventricular block.