AMI
: acute myocardial infarction
ARVC
: arrhythmogenic right ventricular cardiomyopathy
BrS
: Brugada syndrome
CACS
: coronary artery calcium score
CAD
: coronary artery disease
ChD
: Chagas heart disease
CMR
: cardiac magnetic resonance
CPVT
: catecholaminergic polymorphic ventricular tachycardia
CTCA
: computed tomography coronary angiography
CV
: cardiovascular
DCM
: dilated cardiomyopathy
EAPCR
: European Association for Cardiovascular Prevention and Rehabilitation
HCM
: hypertrophic cardiomyopathy
LGE
: late gadolinium enhancement
LQTS
: long QT syndrome
LV/RV
: left/right ventricle
LVH
: left ventricle hypertrophy
NSVT
: non-sustained ventricular tachycardia
PPE
: preparticipation evaluation
PVC
: premature ventricular contractions
SCA/SCD
: sudden cardiac arrest/death
TTE
: transthoracic echocardiography
VF
: ventricular fibrillation
VT
: ventricular tachycardia
Sudden cardiac death (SCD) associated with athletic activity is a rare but devastating event. Victims are usually young and apparently healthy, and while many of these deaths remain unexplained, a substantial number of victims harbour an underlying and potentially detectable cardiovascular (CV) disease.1–4 The vast majority of these events are due to malignant tachyarrhythmias, usually ventricular fibrillation (VF) or ventricular tachycardia (VT) degenerating into ventricular fibrillation (VF), occurring in individuals with arrhythmogenic disorders (e.g. hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, channelopathies). Intensive exercise training and competitive sport participation is a trigger that may favour insurgence of ominous ventricular tachyarrhythmias in predisposed individuals.5 Consequently, there is a great interest in early identification of at-risk individuals for whom appropriate treatment, followed or not by physical activity adjustment, may be implemented to minimize the risk of SCD. However, the role of pre-participation evaluation (PPE) in athletes as a feasible and efficient strategy to identify individuals at risk has remained controversial. …
Myocardial diseases are associated with an increased risk of potentially fatal cardiac arrhythmias and sudden cardiac death/cardiac arrest during exercise, including hypertrophic cardiomyopathy, dilated cardiomyopathy, left ventricular non-compaction, arrhythmogenic cardiomyopathy, and myo-pericarditis. Practicing cardiologists and sport physicians are required to identify high-risk individuals harbouring these cardiac diseases in a timely fashion in the setting of preparticipation screening or medical consultation and provide appropriate advice regarding the participation in competitive sport activities and/or regular exercise programmes. Many asymptomatic (or mildly symptomatic) patients with cardiomyopathies aspire to participate in leisure-time and amateur sport activities to take advantage of the multiple benefits of a physically active lifestyle. In 2005, The European Society of Cardiology (ESC) published recommendations for participation in competitive sport in athletes with cardiomyopathies and myo-pericarditis. One decade on, these recommendations are partly obsolete given the evolving knowledge of the diagnosis, management and treatment of cardiomyopathies and myo-pericarditis. The present document, therefore, aims to offer a comprehensive overview of the most updated recommendations for practicing cardiologists and sport physicians managing athletes with cardiomyopathies and myo-pericarditis and provides pragmatic advice for safe participation in competitive sport at professional and amateur level, as well as in a variety of recreational physical activities.
Background and Purpose— Elevated serum levels of brain natriuretic peptide (BNP) have been associated with cardioembolic stroke and increased poststroke mortality. We sought to determine whether BNP levels were associated with functional outcome after ischemic stroke. Methods— We measured BNP in consecutive patients aged ≥18 years admitted to our stroke unit between 2002 to 2005. BNP quintiles were used for analysis. Stroke subtypes were assigned using Trial of ORG 10172 in Acute Stroke Treatment criteria. Outcomes were measured as 6-month modified Rankin Scale score (“good outcome”=0–2 versus “poor”) as well as mortality. Multivariate logistic regression was used to assess association between the quintiles of BNP and outcomes. Predictive performance of BNP as compared with clinical model alone was assessed by comparing receiver operating characteristic curves. Results— Of 569 patients with ischemic stroke, 46% were female; mean age was 67.9±15 years. In age- and gender-adjusted analysis, elevated BNP was associated with lower ejection fraction ( P <0.0001) and left atrial dilatation ( P <0.001). In multivariate analysis, elevated BNP decreased the odds of good functional outcome (OR, 0.64; 95% CI, 0.41–0.98) and increased the odds of death (OR, 1.75; 95% CI, 1.36–2.24) in these patients. Addition of BNP to multivariate models increased their predictive performance for functional outcome ( P =0.013) and mortality ( P <0.03) after cardioembolic stroke. Conclusions— Serum BNP levels are strongly associated with cardioembolic stroke and functional outcome at 6 months after ischemic stroke. Inclusion of BNP improved prediction of mortality in patients with cardioembolic stroke.
Introduction: Intracerebral Hemorrhage (ICH) has previously been shown to disproportionately affect African-American (AA) and Hispanic-American (HA) patients compared to White (W). ICH recurrence risk, while a critical determinant of long-term disability and mortality, has not been extensively studies among minority individuals. Hypothesis: We sought to clarify whether AA and HA patients are at higher risk for ICH recurrence, and whether etiological differences exist for rebleeding events in different racial / ethnic groups. Methods: We analyzed data for 1542 ICH survivors enrolled in the Ethnic/Racial Variations of Intracerebral Hemorrhage (ERICH) study, who survived at least three months post-ICH and were followed for at least one year. Participants underwent scheduled follow-up at 10-16, 22-28 and 50-60 weeks after index ICH to identify recurrence events. ICH etiology (primarily hypertensive vs. primarily amyloid related) was determined on the basis of index hemorrhage location, i.e. lobar for amyloid and non-lobar for hypertensive bleeds. Results: We analyzed data for 1542 ICH survivors (W: n=514, AA: n=453, HA: n=565), and identified a total of 42 recurrent ICH events (2.72%). AA patients were at higher risk for ICH recurrence compared to W (3.75% vs. 2.10%, p = 0.012), while HA were not (2.20% vs. 2.10%, p=0.78). Self-identified AA race/ethnicity was associated with greater risk for non-lobar ICH (Hazard Ratio [HR]=2.77, p=0.008) than lobar ICH (HR=1.43, p=0.048). Conclusions: AA ICH survivors are at higher risk for recurrent bleeding, and particularly for non-lobar hypertensive hemorrhages. These findings highlight the need for dedicated studies investigating the biological determinants of ICH recurrence in different racial/ethnic patient populations.
Genetic variants ε2/ε4 within the APOE gene are established risk factors for lobar intracerebral hemorrhage (ICH). Published preliminary data suggest a potential role for APOE ε4 in risk of nonlobar ICH. We therefore investigated the role of APOE in recurrent nonlobar ICH, and sought to clarify whether effects of APOE on circulating lipids mediate this association.Three hundred sixty-three survivors of nonlobar ICH were followed prospectively for ICH recurrence, with APOE genotype determined at enrollment. All participants had clinical, demographic, and laboratory data captured at time of index ICH and during follow-up. Using a multivariate model, we performed association and interaction analyses of the relationships among APOE genotype, lipid levels, and recurrent nonlobar ICH.We observed 29 nonlobar ICH recurrences among 363 survivors. APOE ε4 was associated with recurrent nonlobar ICH (hazard ratio = 1.31; 95% confidence interval = 1.02-2.69; p = 0.038) after adjustment for age/sex/ethnicity and cardiovascular risk factors. Increasing low-density lipoprotein (LDL) levels were associated with decreased risk of recurrent nonlobar ICH (p = 0.027), as were decreasing HDL levels (p = 0.046). LDL levels modified the association of APOE ε4 with recurrent nonlobar ICH (mediation p < 0.05). No associations were identified between APOE ε2 and recurrent nonlobar ICH.APOE ε4 is associated with recurrent ICH in nonlobar brain regions, providing further evidence for its causal role in ICH unrelated to cerebral amyloid angiopathy. LDL levels modulated this effect, suggesting that circulating lipid levels may mediate a portion of the role of APOE ε4 in nonlobar ICH.
Neurocritical care beds are a scarce, valuable resource. The purpose of this pilot study was to quantify discharge delays from the neurologic intensive care unit (NICU) at a tertiary-care teaching hospital and to examine the impact on overall hospital length of stay (LOS). Secondary goals were to evaluate (1) the effect of NICU delays on patient physical/occupational therapy services and (2) the accuracy of clinician estimates of NICU discharge date and hospital LOS.We conducted a prospective cohort study of consecutive patients discharged over 1 month from NICU. A patient was defined to have experienced a delay when deemed medically ready for NICU discharge (ie, floor transfer) but without actual NICU discharge within 8 hours of the ready time.Sixty-five patients were discharged from the NICU with an average delay of 25 hours 51 minutes (median 13 hours 3 minutes), of which 60% (39 of 65) of patients were delayed at least 8 hours, while 25% (16 of 65) were delayed at least 48 hours. The primary reason for delay was lack of floor bed availability. NICU admissions that experienced a delay did not have a significantly longer hospital LOS. Clinician estimates on admission of NICU discharge date were within 24 hours for 63% of admissions.Discharge delays from the NICU were common but did not significantly increase hospital LOS in this cohort. Delays did not have a significant impact on total physical therapy or occupational therapy duration. Clinician estimates of NICU discharge dates were relatively accurate.
The difference between men and women is clear even just by looking at an electrocardiogram: females present higher resting heart rate, a shorter QRS complex length and greater corrected QT interval. The development of these differences from pubertal age onward suggests that sexual hormones play a key role, although their effect is far from being completely understood. Different incidences between sexes have been reported for many arrhythmias, both ventricular and supraventricular, and also for sudden cardiac death. Moreover, arrhythmias are an important issue during pregnancy, both for diagnosis and treatment. Interestingly, cardiovascular structural and electrophysiological remodelling promoted by exercise training enhances this 'gender effect'. Despite all these relevant issues, we lack gender specific recommendations in the current guidelines for electrical therapies for heart rhythm disorders and heart failure. Even more, we continue to see that fewer women are included in clinical trials and are less referred than men for these treatments.
The objective of this study was to assess the level of agreement between stroke subtype classifications made using the Trial of Org 10172 Acute Stroke Treatment (TOAST) and Causative Classification of Stroke (CCS) systems.Study subjects included 13,596 adult men and women accrued from 20 US and European genetic research centers participating in the National Institute of Neurological Disorders and Stroke (NINDS) Stroke Genetics Network (SiGN). All cases had independently classified TOAST and CCS stroke subtypes. Kappa statistics were calculated for the 5 major ischemic stroke subtypes common to both systems.The overall agreement between TOAST and CCS was moderate (agreement rate, 70%; κ = 0.59, 95% confidence interval [CI] 0.58-0.60). Agreement varied widely across study sites, ranging from 28% to 90%. Agreement on specific subtypes was highest for large-artery atherosclerosis (κ = 0.71, 95% CI 0.69-0.73) and lowest for small-artery occlusion (κ = 0.56, 95% CI 0.54-0.58).Agreement between TOAST and CCS diagnoses was moderate. Caution is warranted when comparing or combining results based on the 2 systems. Replication of study results, for example, genome-wide association studies, should utilize phenotypes determined by the same classification system, ideally applied in the same manner.
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