Atrial fibrillation/atrial flutter related mortality trends in the US population 2010-2020: Regional, racial, sex variations.

BACKGROUND: There is an evolving need to evaluate atrial fibrillation/atrial flutter (AF/AFL) mortality trends across races, sexes, geographic regions and urbanization statuses to better understand management inequalities. METHODS: This observational study utilized the Centers for Disease Control and Prevention Wide-Ranging Online Data for Epidemiologic Research (CDC WONDER) database. Mortality rates due to AF/AFL as underlying and contributing causes of death between 2010 and 2020 were investigated. Mortality trends due to AF/AFL as contributing causes of death for different races, sexes, census regions and urbanization statuses were analyzed using annual percentage change (APC), and Joinpoint regression analysis. RESULTS: Mortality from AF/AFL as the underlying cause was increasing across the US until 2016 (APC 4.8%), followed by a plateau 2016-2020 (APC 0.0 %). Conversely, the mortality rate due to AF/AFL as a contributing cause increases 2010-2020 (APC 3.3%). The mortality rate in both sexes significantly increased in almost all groups, with the largest increase seen in Non-Hispanic Black males. Rural areas had a higher mortality rate (36.9 and 22.9 per 100,000 for males and females in 2020, respectively) and higher slope of increase than urban areas in total US population. Non-Hispanic White people had greater mortality than Non-Hispanic Black people; however, Non-Hispanic Black mortality rates are increasing at a faster rate in urban areas. CONCLUSION: AF/AFL as the underlying cause of death has plateaued from 2016 across the US 2010-2020; whilst AF/AFL as contributing cause of death is increasing. Significant discrepancies in mortality rates are identified between races and urbanization status.

Electroanatomic Correlates of Depolarization Abnormalities in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy.

BACKGROUND: Epsilon waves and other depolarization abnormalities in the right precordial leads are thought to represent delayed activation of the right ventricular outflow tract in arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C). However, no study has directly correlated cardiac electrical activation with the surface ECG findings in ARVD/C. METHODS AND RESULTS: Thirty ARVD/C patients (mean age 32.7 ± 11.2 years, 16 men) underwent endocardial and epicardial electroanatomical activation mapping in sinus rhythm. Twelve-lead ECGs were classified into 5 patterns: (1) normal QRS (11 patients); (2) terminal activation delay (TAD) (3 patients); (3) incomplete right bundle branch block (IRBBB) (5 patients); (4) epsilon wave (5 patients); (5) complete right bundle branch block (CRBBB) (6 patients). Timing of local ventricular activation and extent of scar was then correlated with surface QRS. Earliest endocardial and epicardial RV activation occurred on the mid anteroseptal wall in all patients despite the CRBBB pattern on ECG. Total RV activation times increased from normal QRS to prolonged TAD, IRBBB, epsilon wave, and CRBBB, respectively (103.9 ± 5.6, 116.3 ± 6.5, 117.8 ± 2.7, 146.4 ± 16.3, and 154.3 ± 6.3, respectively, P < 0.05). The total epicardial scar area (cm(2) ) was similar among the different ECG patterns. Median endocardial scar burden was significantly higher in patients with epsilon waves even compared with patients with CRBBB (34.3 vs. 11.3 cm(2) , P < 0.01). Timing of epsilon wave corresponded to activation of the subtricuspid region in all patients. CONCLUSION: We found that epsilon waves are often associated with severe conduction delay and extensive endocardial scarring in addition to epicardial disease. The timing of epsilon waves on surface ECG correlated with electrical activation of the sub-tricuspid region.

2015 update on the diagnosis and management of arrhythmogenic right ventricular cardiomyopathy.

PURPOSE OF REVIEW: This review will discuss the recent advances in the diagnosis and management of arrhythmogenic right ventricular cardiomyopathy (ARVC). RECENT FINDINGS: Since the first detailed clinical description of the disease in 1982, we have learned much about the genetics, pathophysiology, diagnosis, and management of ARVC. We now appreciate that pathogenic mutations in desmosomal genes are the most common genetic finding. Although the right ventricle is mostly affected, left ventricular involvement is being increasingly recognized. Electrical instability precipitating sudden cardiac death often presents before structural abnormalities, and therefore early accurate diagnosis is of utmost importance. The broad spectrum of phenotypic variation, age-related penetrance, and lack of a definitive diagnostic test make the clinical diagnosis challenging. The diagnosis is made by fulfilling the 2010 Task Force criteria. Today, genetic testing and cardiac MRI play an important role in the diagnosis. Implantable cardioverter defibrillator implantation is the only lifesaving therapy available today for a subset of patients. In patients with recurrent ventricular arrhythmias, epicardial catheter ablation has demonstrated improved outcomes compared with endocardial ablation. Exercise restriction may delay the progression of disease. SUMMARY: ARVC is predominantly associated with mutations in desmosomal genes with incomplete penetrance and variable expressivity. Ventricular electrical instability is the hallmark of ARVC, often occurring before structural abnormalities. Goals in the evaluation and management of ARVC are early diagnosis, risk stratification for sudden cardiac death, minimizing ventricular arrhythmias, and delaying the progression of disease.

All-cause mortality due to conduction abnormalities in the United States: sex, racial, and geographic variations from 1999 to 2022.

BACKGROUND: Mortality related to conduction abnormalities in the US population is not well-documented. Population-based stratification approaches can improve public health policies and targeted strategies. OBJECTIVE: To evaluate all-cause mortality related to conduction abnormalities in the US population METHODS: The CDC WONDER database was utilized to calculate the Age-Adjusted Mortality Rate (AAMR) per 100,000 individuals above 35 years old related to conduction abnormalities between 1999 and 2022. RESULTS: A total of 207,861 deaths were attributed to conduction abnormalities throughout the study period with 56,186 of these deaths occurring between 2020 and 2022. All-cause mortality related to conduction abnormalities has increased during the past decade with an exponential growth in 2020-2021 (COVID-19 era; Annual Percent Change (APC) of 16.6% per year). Although the mortality rates decreased in 2022, they remained elevated compared to 2019-2020. Throughout the past two decades, males consistently exhibited higher mortality rates than females, with the rate in 2022 being 1.5 times higher (AAMR 11.4 vs 7.0 per 100,000). Non-Hispanic Black patients experienced a significantly higher mortality rate compared to non-Hispanic White individuals in the study period (AAMR 13.7 vs. 8.6 per 100,000 in 2022). In the past two decades, mortality has been persistently higher in rural and small-medium-sized metro areas than in large metro urban areas. CONCLUSIONS: Mortality rates related to conduction abnormalities have increased over the past decade, and persistent disparities have been observed. These data suggest that continued innovative outreach approaches and engagement with under-represented populations remain essential.

Response to atrial extrastimulus during supraventricular tachycardia: what is the mechanism?

We describe a case illustrating the potential challenges in distinguishing AV nodal reentry tachycardia (AVNRT) from automatic junctional tachycardia (JT). While an early atrial extrastimulus advanced the next His and ventricular depolarization without tachycardia termination, suggesting JT, other features indicated the correct diagnosis of AVNRT. This teaching case demonstrates a novel exception to a recently reported diagnostic pacing maneuver and illustrates the importance of considering response to multiple maneuvers in reaching a diagnosis of SVT mechanism.

Phrenic nerve injury: An underrecognized and potentially preventable complication of pulmonary vein isolation using a wide-area circumferential ablation approach.

INTRODUCTION: Phrenic nerve injury (PNI) is a well-known, although uncommon, complication of pulmonary vein isolation (PVI) using radiofrequency energy. Currently, there is no consensus about how to avoid or minimize this injury. The purpose of this study was to determine how often the phrenic nerve, as identified using a high-output pacing, lies along the ablation trajectory of a wide-area circumferential lesion set. We also sought to determine if PVI can be achieved without phrenic nerve injury by modifying the ablation lesion set so as to avoid those areas where phrenic nerve capture (PNC) is observed. METHODS AND RESULTS: We prospectively enrolled 100 consecutive patients (age 61.7 ± 9.2 years old, 75 men) who underwent RF PVI using a wide-area circumferential ablation approach. A high-output (20 mA at 2 milliseconds) endocardial pacing protocol was performed around the right pulmonary veins and the carina where a usual ablation lesion set would be made. A total of 30% of patients had PNC and required modification of ablation lines. In the group of patients with PNC, the carina was the most common site of capture (85%) followed by anterior right superior pulmonary vein (RSPV) (70%) and anterior right inferior pulmonary vein (RIPV) (30%). A total of 25% of PNC group had capture in all 3 (RSPV, RIPV, and carina) regions. There was no difference in the clinical characteristics between the groups with and without PNC. RF PVI caused no PNI in either group. CONCLUSION: High output pacing around the right pulmonary veins and the carina reveals that the phrenic nerve lies along a wide-area circumferential ablation trajectory in 30% of patients. Modification of ablation lines to avoid these sites may prevent phrenic nerve injury during RF PVI.

Mutation-positive arrhythmogenic right ventricular dysplasia/cardiomyopathy: the triangle of dysplasia displaced.

INTRODUCTION: The traditional description of the Triangle of Dysplasia in Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) predates genetic testing and excludes biventricular phenotypes. METHODS AND RESULTS: We analyzed Cardiac Magnetic Resonance (CMR) studies of 74 mutation-positive ARVD/C patients for regional abnormalities on a 5-segment RV and 17-segment LV model. The location of electroanatomic endo- and epicardial scar and site of successful VT ablation was recorded in 11 ARVD/C subjects. Among 54/74 (73%) subjects with abnormal CMR, the RV was abnormal in almost all (96%), and 52% had biventricular involvement. Isolated LV abnormalities were uncommon (4%). Dyskinetic basal inferior wall (94%) was the most prevalent RV abnormality, followed by basal anterior wall (87%) dyskinesis. Subepicardial fat infiltration in the posterolateral LV (80%) was the most frequent LV abnormality. Similar to CMR data, voltage maps revealed scar (<0.5 mV) in the RV basal inferior wall (100%), followed by the RV basal anterior wall (64%) and LV posterolateral wall (45%). All 16 RV VTs originated from the basal inferior wall (50%) or basal anterior wall (50%). Of 3 LV VTs, 2 localized to the posterolateral wall. In both modalities, RV apical involvement never occurred in isolation. CONCLUSION: Mutation-positive ARVD/C exhibits a previously unrecognized characteristic pattern of disease involving the basal inferior and anterior RV, and the posterolateral LV. The RV apex is only involved in advanced ARVD/C, typically as a part of global RV involvement. These results displace the RV apex from the Triangle of Dysplasia, and provide insights into the pathophysiology of ARVD/C.

Gender, Age, and Regional Disparities in the Incidence and Mortality Trends of Infective Endocarditis in the United States Between 1990 and 2019.

The incidence of infective endocarditis (IE) has increased globally in the past decades, including in the United States. However, little is known about the differences in trends across states, gender, and age groups within the United States. Using the Global Burden of Disease database, we analyzed the incidence and mortality trends of IE in the United States between 1990 and 2019 using Joinpoint regression analyses, and compared between states, gender, and age groups. The age-standardized incidence rate (ASIR) of IE in the United States increased from 10.2/100,000 population in 1990 to 14.4 in 2019. The increase in ASIR was greater among men than women (45.8% vs 34.1%). The incidence increase was driven by 55+ year-olds (112.7% increase), with rapid increases in the 1990s and early 2000s, followed by a plateau around the mid-2000s. In contrast, the incidence among 5-to-19-year-olds decreased by -36.6% over the 30-year period. The incidence increased among all age groups in the last 5 years of observation (2015 to 2019), with the largest increase in 5-to-19-year-olds (3.3% yearly). The 30-year increase in ASIR was greatest in Utah (66.2%) and smallest in California (30.2%). The overall age-standardized mortality attributable to IE increased in the United States by 126% between 1990 and 2019 versus 19.6% globally. In conclusion, although the overall incidence and mortality of IE increased over the past 30 years in the United States, there are significant differences between regions, gender, and age groups. These findings indicate unevenly distributed disease burden of IE across the nation.

The value of defibrillator far-field electrograms for ablation of idiopathic ventricular fibrillation.

We report a case of idiopathic ventricular fibrillation treated by catheter ablation of the monomorphic initiating premature beat. The initiating focus was identified using intacardiac defibrillator electrograms (EGMs).

Demographic and State-Level Trends in Mortality Due to Ischemic Heart Disease in the United States from 1999 to 2019.

Although there have been advances in ischemic heart disease (IHD) care, variation in IHD-related mortality trends across the United States has not been well described. We used the Centers for Disease Control and Prevention's Wide-ranging Online Data for Epidemiologic Research database to evaluate variation in IHD-related mortality for demographic groups in the United States between 1999 and 2019. Age-adjusted mortality rates (AAMRs) were stratified by gender, race, Hispanic ethnicity, and US state. Crude mortality rates were evaluated using 10-year age groups. IHD-related AAMRs decreased from 195 to 88 per 100,000 nationally, with slower a decrease from 2010 to 2019 (average annual percent change [AAPC] -2.6% [95% confidence interval -2.9% to -2.2%]) compared with 2002 to 2010 (AAPC -5.3% [95% confidence interval -5.6% to -4.9%]). All groups had decreases in AAMRs, although Black populations persistently had the highest AAMR, and women had greater relative decreases than men. AAPC was -3.7% for White men, -4.7% for White women, -3.9% for Black men, -4.9% for Black women, -4.1% for Hispanic men, and -5.1% for Hispanic women. Populations ≥65 years had greater relative mortality decreases than populations <65 years. The median AAMR (2019) and AAPC (1999 to 2019) across states was 86 (range 58 to 134) and -3.8% (range -1.7% to -4.8%), respectively. In conclusion, declines in IHD-related mortality have slowed in the United States, with a significant geographic variation. Black populations persistently had the highest AAMRs, and decreases were relatively greater for women and populations ≥65 years. The impact of demographics and geography on IHD should be further explored and addressed as part of public health measures.

Cardiogenic shock related cardiovascular disease mortality trends in US population: Heart failure vs. acute myocardial infarction as contributing causes.

BACKGROUND: Observational and trial data have revealed significant improvement in cardiogenic shock (CS) mortality due to acute myocardial infarction (AMI) after introducing early coronary revascularization. Less is known about CS mortality due to heart failure (HF), which is increasingly recognized as a distinct entity from AMI-CS. METHODS AND RESULTS: In this nationwide observational study, the CDC WONDER database was used to identify national trends in age-adjusted mortality rates (AAMR) due to CS (HF vs. AMI related) per 100,000 people aged 35-84. AAMR from AMI-CS decreased significantly from 1999 to 2009 (AAPC: -6.9% [95%CI -7.7, -6.1]) then stabilized from 2009 to 2020. By contrast, HF-CS associated AAMR rose steadily from 2009 to 2020 (AAPC: 13.3% [95%CI 11.4,15.2]). The mortality rate was almost twice as high in males compared to females in both AMI-CS and HF-CS throughout the study period. HF-CS mortality in the non-Hispanic Black population is increasing more quickly than that of the non-Hispanic White population (AAMR in 2020: 4.40 vs. 1.97 in 100,000). The AMI-CS mortality rate has been consistently higher in rural than urban areas (30% higher in 1999 and 28% higher in 2020). CONCLUSIONS: These trends highlight the fact that HF-CS and AMI-CS represent distinct clinical entities. While mortality associated with AMI-CS has primarily declined over the last two decades, the mortality related to HF-CS has increased significantly, particularly over the last decade, and is increasing rapidly among individuals younger than 65. Accordingly, a dramatic change in the demographics of CS patients in modern intensive care units is expected.

What Is the Response Seen During Para-Hisian Pacing?

We present an interesting tracing of para-Hisian pacing in a 45-year-old man with an episode of narrow complex tachycardia and past recurrent palpitations.

Cardiac Resynchronization and Circulating Markers of Sarcoplasmic Reticulum Calcium Handling and Sudden Death Risk.

Cardiac resynchronization therapy (CRT) can improve heart function and decrease arrhythmic events. We tested whether CRT altered circulating markers of calcium handling and sudden death risk. Circulating cardiac sodium channel messenger RNA (mRNA) splicing variants indicate arrhythmic risk, and a reduction in sarco/endoplasmic reticulum calcium adenosine triphosphatase 2a (SERCA2a) is thought to diminish contractility in heart failure. CRT was associated with a decreased proportion of circulating, nonfunctional sodium channels and improved SERCA2a mRNA expression. Patients without CRT did not have improvement in the biomarkers. These changes might explain the lower arrhythmic risk and improved contractility associated with CRT.

Incidence and Mortality Trends of Atrial Fibrillation/Atrial Flutter in the United States 1990 to 2017.

Atrial fibrillation (AF) and flutter (AFL) are the most common clinically significant arrhythmias in older adults with an increasing disease burden due to an aging population. However, up-to-date trends in disease burden and regional variation remain unknown. In an observational study utilizing the Global Burden of Disease (GBD) database, age-standardized mortality and incidence rates for AF overall and for each state in the United States (US) from 1990 to 2017 were determined. All analyses were stratified by gender. The relative change in age-standardized incidence rate (ASIR) and age-standardized death rate (ASDR) over the observation period were determined. Trends were analyzed using Joinpoint regression analysis. The mean ASIR per 100,000 population for men was 92 (+/-8) and for women was 62 (+/-5) in the US in 2017. The mean ASDR per 100,000 population for men was 5.8 (+/-0.3) and for women was 4.4 (+/-0.4). There were progressive increases in ASIR and ASDR in all but 1 state. The states with the greatest percentage change in incidence were New Hampshire (+13.5%) and Idaho (+16.0%) for men and women, respectively. The greatest change regarding mortality was seen in Mississippi (+26.3%) for men and Oregon (+53.8%) for women. In conclusion these findings provide updated evidence of increasing AF and/or AFL incidence and mortality on a national and regional level in the US, with women experiencing greater increases in incidence and mortality rates. This study demonstrates that the public health burden related to AF in the United States is progressively worsening but disproportionately across states and among women.

The oxidized phospholipids linked to human apolipoprotein(a) do not derive from circulating low-density lipoproteins and are probably of cellular origin.

Lipoprotein (a) [Lp(a)], a cardiovascular risk factor, is a low-density lipoprotein (LDL) variant shown to bind to oxidized phospholipids (oxPLs); however, its binding mode and origin have not been clearly established. We isolated both LDL and Lp(a) from the plasma of a population of high-Lp(a) subjects and in each Lp(a) particle separated apolipoprotein(a) [apo(a)], from the LDL component, Lp(a(-)). These products were assayed by an ELISA using monoclonal antibody T15 with a known specificity for oxPLs. In each subject, the T15 reactivity was confined to apo(a). Moreover, the amount of oxPL bound to apo(a) was unaffected by plasma Lp(a) levels and apo(a) size polymorphism. We have previously shown that kringle V (KV) is the site of oxPL linkage in human apo(a). In this work, we expressed in human embryonic kidney cells a KV-containing recombinant that, when purified from the medium, contained oxPLs. In summary, in human plasma Lp(a), the oxPLs are located in apo(a) and not in the circulating LDLs, suggesting a cellular origin. This latter concept is supported by the studies in which an expressed KV-containing apo(a) microdomain exhibited oxPL reactivity. Thus, apo(a) can undergo potentially pathogenic posttranslational modifications in a cellular environment able to generate oxPL.

Implications of family history of myocardial infarction in young women.

BACKGROUND: Family history of premature myocardial infarction (FHMI) may be a useful marker of cardiovascular disease (CVD) risk in young subjects, but comparisons of its implications for CVD risk factor burden, prevalent atherosclerosis, and risk awareness between young men and women have not been reported. METHODS: We analyzed data from 2404 young subjects with ages 30 to 50 in the Dallas Heart Study, which is a population-based study. Family history of premature MI was defined as a first-degree relative with myocardial infarction (MI) before age 50 (men) or 55 (women). Coronary artery calcification was measured by computed tomography scan, and perceived lifetime risk of MI was assessed by questionnaire. Analyses were sex-stratified. RESULTS: Women with versus without FHMI had an increased composite risk factor burden (> or = 2 CVD risk factors, 49.1% vs 39.1%; P < .001), an association not seen in men (P = .6). Family history of premature MI was independently associated with coronary artery calcification among women (adjusted odds ratio, 2.0; 95% confidence interval, 1.0-4.1) but not among men (adjusted odds ratio, 1.7; 95% confidence interval, 0.9-3.2). A higher proportion of subjects with FHMI versus no FHMI perceived their lifetime risk of MI to be at > or = average in women (59.7% vs 47.4%; P < .001) and men (75.0% vs 48.3%; P = .004), with the increment greatest among men (P interaction = .02). CONCLUSIONS: Despite a stronger association with CVD risk factors and atherosclerosis prevalence with FHMI among young women compared with men, young women with FHMI demonstrated less CVD risk awareness and worse lifestyle choices. Family history of premature MI may be an especially useful risk assessment tool in young women, and greater efforts are needed to promote CVD risk awareness among young women with FHMI.

Relation of family history of myocardial infarction and the presence of coronary arterial calcium in various age and risk factor groups.

Family history of myocardial infarction (FHMI) is an independent risk factor for cardiovascular (CV) events but may be more informative in certain subgroups. The association between FHMI and the presence of coronary artery calcium (CAC) was examined in various age and risk factor groups in the Dallas Heart Study (DHS), a population-based probability sample of subjects aged 30 to 65 years. Analyses were stratified by age (with the young group composed of men aged <45 years and women aged <55 years) and by the presence of 0, 1, 2, or >2 CV risk factors. In the overall cohort of 2,743 subjects, FHMI was an independent predictor of CAC (adjusted odds ratio 1.3, 95% confidence interval 1.1 to 1.7), attributable to an independent association between FHMI and CAC in the young group (adjusted odds ratio 1.5, 95% confidence interval 1.0 to 2.1) that was not evident in the older subset (adjusted odds ratio 1.2, 95% confidence interval 0.91 to 1.6, interaction p = 0.02). In the young cohort, the association between FHMI and CAC was particularly robust in those with > or = 2 risk factors (FHMI-by-risk factor interaction p = 0.04). In older subjects, FHMI was not associated with CAC for any risk factor category (p >0.05 for each). In conclusion, this study suggests that FHMI is a more important predictor of atherosclerosis in young compared with older adults and, among the young, in those with multiple CV risk factors.

Endothelial progenitor cell mobilization after percutaneous coronary intervention.

BACKGROUND: In animal models, circulating endothelial progenitor cells (EPC) have been shown to participate in repair of damaged or degenerating vascular surfaces. In humans, reduced EPC counts correlate with cardiovascular risk and disease outcome; yet it has been difficult to establish that EPC are in fact mobilized in response to vascular injury as a physiologic response. We therefore studied early (<12h) mobilization of EPCs into the peripheral circulation after a defined vascular manipulation, percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS) and non-ACS patients. METHODS AND RESULTS: CD34/CD31 positive EPC colony forming units (EPC-CFU) were quantified by a blinded observer in peripheral blood samples from eight control patients with angiographically normal coronary arteries, and in 30 patients with coronary artery lesions before and 12h after PCI. All patients (n=38) had one or more CV risk factors. Ten patients presented with acute coronary syndrome (PCI(ACS)), and the rest (n=20) underwent elective PCI (PCI(Elect)). Despite the presence of an acute coronary syndrome, patients in the PCI(ACS) group did not present with increased EPC-CFU compared with either the PCI(Elect) or control groups (P>0.05). In addition, EPC-CFU (colonies/ml blood) increased significantly in the PCI(Elect) group after stent placement (11.8+1.6 before versus 16.5+1.9 after, P=0.0009), while in contrast, PCI did not stimulate EPC mobilization in patients in the PCI(ACS) group (9.6+3.2 before versus 6.5+1.8, P=0.20). We found a higher presenting vascular endothelial growth factor (VEGF) level in the PCI(Elect) group compared to PCI(ACS) (78.7+25.2 versus 15.3+7.9 pg/ml blood, P=0.02). However, VEGF levels increased after PCI only in the PCI(ACS) group (15.3+7.9 to 133.3+27.5 pg/ml, P=0.003) and not in the PCI(Elect) group (78.7+25.2 to 79.7+12.2 pg/ml, P=0.97). CONCLUSION: Our findings suggest that focal coronary endothelial injury as a result of PCI triggers early mobilization of EPC into the peripheral circulation in patients presenting for an elective PCI, without a corresponding rise in VEGF levels. In contrast, patients with an acute coronary syndrome fail to respond to PCI with early EPC mobilization despite a significant rise in VEGF. The results of the present study may suggest a novel mechanism for early EPC augmentation after PCI.

The association of left atrial low-voltage regions on electroanatomic mapping with low attenuation regions on cardiac computed tomography perfusion imaging in patients with atrial fibrillation.

BACKGROUND: Previous studies have shown that contrast-enhanced multidetector computed tomography (CE-MDCT) could identify ventricular fibrosis after myocardial infarction. However, whether CE-MDCT can characterize atrial low-voltage regions remains unknown. OBJECTIVE: The purpose of this study was to examine the association of CE-MDCT image attenuation with left atrial (LA) low bipolar voltage regions in patients undergoing repeat ablation for atrial fibrillation recurrence. METHODS: We enrolled 20 patients undergoing repeat ablation for atrial fibrillation recurrence. All patients underwent preprocedural 3-dimensional CE-MDCT of the LA, followed by voltage mapping (>100 points) of the LA during the ablation procedure. Epicardial and endocardial contours were manually drawn around LA myocardium on multiplanar CE-MDCT axial images. Segmented 3-dimensional images of the LA myocardium were reconstructed. Electroanatomic map points were retrospectively registered to the corresponding CE-MDCT images. RESULTS: A total of 2028 electroanatomic map points obtained in sinus rhythm from the LA endocardium were registered to the segmented LA wall CE-MDCT images. In a linear mixed model, each unit increase in the local image attenuation ratio was associated with 25.2% increase in log bipolar voltage (P = .046) after adjusting for age, sex, body mass index, and LA volume, as well as clustering of data by patient and LA regions. CONCLUSION: We demonstrate that the image attenuation ratio derived from CE-MDCT is associated with LA bipolar voltage. The potential ability to image fibrosis via CE-MDCT may provide a useful alternative in patients with contraindications to magnetic resonance imaging.