Risk Of Sudden Cardiac Death Research Articles

Ondansetron and the Risk of Sudden Cardiac Death among Individuals Receiving Maintenance Hemodialysis.

Individuals receiving hemodialysis have high incidence of sudden cardiac death and are susceptible to QT interval prolonging medication-related cardiac complications. Ondansetron, an antiemetic with known QT prolonging potential, is associated with fatal arrythmias in the general population when administered intravenously. The cardiac safety of ondansetron in the hemodialysis population is unknown. We conducted a new-user, active-comparator, cohort study using US Renal Data System data (2012-2019) to examine the association between the initiation of oral ondansetron vs. antiemetics with lesser QT prolonging potential (promethazine, metoclopramide or prochlorperazine) and the 10-day risk of sudden cardiac death among individuals receiving hemodialysis. We used inverse probability of treatment weighted survival models to estimate adjusted hazard ratios (aHRs), risk differences (aRDs), and 95% confidence intervals (CIs). We used an intention-to-treat approach in which non-sudden cardiac death was considered a competing event. We examined additional cardiac outcomes in secondary analyses. Of the 119,254 study patients, 64,978 (54.5%) initiated ondansetron, and 54,276 (45.5%) initiated a comparator antiemetic. Initiation of ondansetron versus a comparator antiemetic was associated with higher relative and absolute 10-day risks of sudden cardiac death, aHR (95% CI) = 1.44 (1.08, 1.93); aRD (95% CI) = 0.06% (0.01%, 0.11%). The number needed to harm was 1,688. Analyses of additional cardiac outcomes yielded similar findings. Compared with initiation of antiemetics with lesser QT prolonging potential, initiation of ondansetron was associated with higher short-term cardiac risks among people receiving hemodialysis.

History of clinical electrophysiology in diagnosing and treatment monitoring of high ventricular vulnerability

The paper presents the history of hope from 1980-1995 to predict the risk of sudden arrhythmic death using electrophysiologic techniques in individual patients. Even if this prediction seems possible in selected highly risk cohorts, many more patients will die in ventricular arrhythmia without fulfilling the criteria. Ultimately, high risk of sudden cardiac death can be predicted in selected patient groups, but not in the majority of patients at risk. It is ahistory of dashed hope.

Arrhythmic Mitral Valve Prolapse and Sports Activity: Pathophysiology, Risk Stratification, and Sports Eligibility Assessment.

Although mitral valve prolapse (MVP) is the most prevalent valvular abnormality in Western countries and generally carries a good prognosis, a small subset of patients is exposed to a significant risk of malignant ventricular arrhythmias (VAs) and sudden cardiac death (SCD), the so-called arrhythmic MVP (AMVP) syndrome. Recent work has emphasized phenotypical risk features of severe AMVP and clarified its pathophysiology. However, the appropriate assessment and risk stratification of patients with suspected AMVP remains a clinical conundrum, with the possibility of both overestimating and underestimating the risk of malignant VAs, with the inappropriate use of advanced imaging and invasive electrophysiology study on one hand, and the catastrophic occurrence of SCD on the other. Furthermore, the sports eligibility assessment of athletes with AMVP remains ill defined, especially in the grey zone of intermediate arrhythmic risk. The definition, epidemiology, pathophysiology, risk stratification, and treatment of AMVP are covered in the present review. Considering recent guidelines and expert consensus statements, we propose a comprehensive pathway to facilitate appropriate counseling concerning the practice of competitive/leisure-time sports, envisioning shared decision making and the multidisciplinary "sports heart team" evaluation of borderline cases. Our final aim is to encourage an active lifestyle without compromising patients' safety.

Anti-Arrhythmic Effects of Heart Failure Guideline-Directed Medical Therapy and Their Role in the Prevention of Sudden Cardiac Death: From Beta-Blockers to Sodium-Glucose Cotransporter 2 Inhibitors and Beyond.

Sudden cardiac death (SCD) accounts for a substantial proportion of mortality in heart failure with reduced ejection fraction (HFrEF), frequently triggered by ventricular arrhythmias (VA). This review aims to analyze the pathophysiological mechanisms underlying VA and SCD in HFrEF and evaluate the effectiveness of guideline-directed medical therapy (GDMT) in reducing SCD. Beta-blockers, angiotensin receptor-neprilysin inhibitors, and mineralocorticoid receptor antagonists have shown significant efficacy in reducing SCD risk. While angiotensin-converting enzyme inhibitors and angiotensin receptor blockers exert beneficial impacts on the renin-angiotensin-aldosterone system, their direct role in SCD prevention remains less clear. Emerging treatments like sodium-glucose cotransporter 2 inhibitors show promise but necessitate further research for conclusive evidence. The favorable outcomes of those molecules on VA are notably attributable to sympathetic nervous system modulation, structural remodeling attenuation, and ion channel stabilization. A multidimensional pharmacological approach targeting those pathophysiological mechanisms offers a complete and synergy approach to reducing SCD risk, thereby highlighting the importance of optimizing GDMT for HFrEF. The current landscape of HFrEF pharmacotherapy is evolving, with ongoing research needed to clarify the full extent of the anti-arrhythmic benefits offered by both existing and new treatments.

Effect of SGLT-2 inhibitors on arrhythmia events: insight from an updated secondary analysis of > 80,000 patients (the SGLT2i—Arrhythmias and Sudden Cardiac Death)

ObjectiveWe aimed to assess the effect of SGLT2i on arrhythmias by conducting a meta-analysis using data from randomized controlled trials(RCTs).BackgroundSodium-glucose co-transporter 2 inhibitors (SGLT2i) have shown cardioprotective effects via multiple mechanisms that may also contribute to decrease arrhythmias risk.MethodsWe searched in databases (PubMed, Embase, Cochrane Library, and clinicaltrials.gov) up to April 2023. RCTs comparing SGLT2i with placebo were included. The effects of SGLT2i on atrial fibrillation(AF), atrial flutter(AFL), composite AF/AFL, ventricular fibrillation(VF), ventricular tachycardia(VT), ventricular extrasystoles(VES), sudden cardiac death(SCD) and composite VF/VT/SCD were evaluated.Results33 placebo-controlled RCTs were included, comprising 88,098 patients (48,585 in SGLT2i vs. 39,513 in placebo). The mean age was 64.9 ± 9.4 years, 63.0% were male. The mean follow-up was 1.4 ± 1.1 years. The pooled-results showed that SGLT2i was associated with a significantly lower risk of AF [risk ratio(RR): 0.88, 95% confidence interval(CI) 0.78–1.00, P = 0.04] and composite AF/AFL (RR: 0.86, 95%CI 0.77–0.96, P = 0.01). This favorable effect appeared to be substantially pronounced in patients with HFrEF, male gender, dapagliflozin, and > 1 year follow-up. For SCD, only in heart failure patients, SGLT2i were found to be associated with a borderline lower risk of SCD (RR: 0.67, P = 0.05). No significant effects of SGLT2i on other ventricular arrhythmic outcomes were found.ConclusionsSGLT2i lowers the risks of AF and AF/AFL, and this favorable effect appeared to be particularly pronounced in patients with HFrEF, male gender, dapagliflozin, and longer follow-up (> 1 year). SGLT2i lowers the risk of SCD only in heart failure patients.Graphical

Ventricular Arrhythmias and Hemodynamic Collapse During Acute Coronary Syndrome- Increased Risk for Sudden Cardiac Death?

In acute phase of acute coronary syndrome (ACS), ventricular tachycardia (VT) and/or ventricular fibrillation (VF) leading to resuscitation are not considered to be associated with increased long-term sudden cardiac death (SCD) because the cause - acute ischemia - is believed to be reversible.Aim of this study was to investigate whether ventricular arrhythmias leading to sudden cardiac arrest during ACS associate with the risk of incident SCD in patients with normal or mildly impaired left ventricular ejection fraction (LVEF). This study is based on a retrospective analysis of all 8,062 consecutive ACS patients undergoing coronary angiography with baseline LVEF ≥40% between 2007-2018 (follow-up until December 31st, 2021). The primary outcome was SCD equivalent life-threatening ventricular arrhythmias (LTVA) composing of true SCDs, aborted SCDs by successful resuscitation or appropriate ICD therapy. The risk of sudden LTVA was estimated with multivariate subdistribution hazard model using other deaths as competing events. Two-hundred and thirteen (n=211, 2.6%) patients suffered acute phase VF/VT leading to resuscitation and survived to discharge and most happened before angiography (80.6%, N=170) and were VF (92.9%, N=196). During a median follow-up of 7.6 years, 3.9% (N=316) of all the patients had LTVA (10.0% in VF/VT group vs 3.8% in other patients). VF/VTs during ACS associated with an increased risk for future SCD (HR 3.07; 95% CI 1.94-4.85, p<0.001). Most LTVAs occurred in patients without ICDs. VF/VT in ACS associates with remarkably high long-term risk for SCD in patients with LVEF ≥40%.

Development of the NOCSAE Standard to Reduce the Risk of Commotio Cordis.

Commotio cordis, sudden cardiac death (SCD) caused by relatively innocent impact to the chest, is one of the leading causes of SCD in sports. Commercial chest protectors have not been demonstrated to mitigate the risk of these SCDs. To develop a standard to assess chest protectors, 4 phases occurred. A physiological commotio cordis model was utilized to assess variables that predicted for SCD. Next, a surrogate model was developed based on data from the physiological model, and the attenuation in risk was assessed. In the third phase, this model was calibrated and validated. Finally, National Operating Committee on Standards for Athletic Equipment adopted the standard and had an open review process with revision of the standard over 3 years. Of all variables, impact force was the most robust at predicting SCD. Chest wall protectors which could reduce the force of impact to under thresholds were predicted to reduce the risk of SCD. The correlation between the experimental model and the mechanical surrogate ranged from 0.783 with a lacrosse ball at 30 mph to 0.898 with a baseball at 50 mph. The standard was licensed to National Operating Committee on Standards for Athletic Equipment which initially adopted the standard in January 2018, and finalized in July 2021. An effective mechanical surrogate based on physiological data from a well-established model of commotio cordis predicts the reduction in SCD with chest protectors. A greater reduction in force provides a great degree of protection from commotio cordis. This new National Operating Committee on Standards for Athletic Equipment standard for chest protectors should result in a significant reduction in the risk of commotio cordis on the playing field.

Connecting the Dots: Heart Failure and Insomnia

Introduction and aim. This study investigates the relationship between heart failure (HF) and insomnia, focusing on this two-way association’s clinical significance, epidemiology, and management.&#x0D; Material and methods. Literature available in November 2023 was searched using Pubmed, Medline, Google Scholar, and Europe PMC with keywords associated with Heart Failure, Insomnia, and related pharmaceuticals. 69 articles were included.&#x0D; Analysis of the literature. Insomnia is associated with higher mortality and a potential risk of sudden cardiac death, particularly in individuals with HF. Treatment is challenging and side effects can worsen the symptoms of HF. The use of benzodiazepines in HF patients raises concerns about cardiovascular risks, prompting the exploration of other medications like nonbenzodiazepines, antidepressants with sedative effects, and histamine receptor antagonists. On the other hand, HF is also a condition that affects sleep quality. Drugs including ACE-I, beta-blockers, MRA, and SGLT2i are essential for its treatment. Some of them may have an impact on the intensity of insomnia.&#x0D; Conclusion. Considering the impact of insomnia medications on heart failure outcomes and vice versa is necessary. It is important to consider all aspects when treating these two conditions simultaneously.

Genetic Characterization of Dilated Cardiomyopathy in Romanian Adult Patients.

Dilated cardiomyopathy (DCM) represents a group of disorders affecting the structure and function of the heart muscle, leading to a high risk of heart failure and sudden cardiac death (SCD). DCM frequently involves an underlying genetic etiology. Genetic testing is valuable for risk stratification, treatment decisions, and family screening. Romanian population data on the genetic etiology of DCM are lacking. We aimed to investigate the genetic causes for DCM among Romanian adult patients at tertiary referral centers across the country. Clinical and genetic investigations were performed on adult patients presenting to tertiary hospitals in Romania. The genetic investigations used next-generation sequencing panels of disease-associated DCM genes. A total of 122 patients with DCM underwent genetic testing. The mean age at DCM diagnosis was 41.6 ± 12.4 years. The genetic investigations identified pathogenic or likely pathogenic variants in 50.8% of participants, while 25.4% had variants of unknown significance. Disease-causing variants in 15 genes were identified in people with DCM, with 31 previously unreported variants. Variants in TTN, LMNA, and DSP explained 75% of genetic causes for DCM. In total, 52.4% of patients had a family history of DCM/SCD. Left ventricular ejection fraction of <35% was observed in 41.9% of patients with disease-causing variants and 55% with negative or uncertain findings. Further genotype-phenotype correlations were explored in this study population. The substantial percentage (50.8%) of disease-causing variants identified in patients with DCM acknowledges the importance of genetic investigations. This study highlights the genetic landscape in genes associated with DCM in the Romanian population.

Prior history of atrial fibrillation and arrhythmic outcomes: Data from the WEARIT-II prospective registry.

Wearable cardioverter defibrillator (WCD)is utilized in patients with assumed but not yet confirmed risk for sudden cardiac death (SCD).Many of these patients also present with atrial fibrillation (AF).However, the rate of WCD-detected ventricular or atrial arrhythmia events in this specific high-risk cohort is not well understood. In WEARIT-II,the cumulative probability of any sustained or nonsustained VT/VF(WCD-treatedand nontreated), and atrial/supraventricular arrhythmias during WCD use was assessed using the Kaplan-Meier method by prior AF, with comparisons by the log-rank test. The incidence of ventricular and atrial arrhythmia events were expressed as events per 100 patient-years, and were analyzed by prior AF using negative binomial regression. WEARIT-IIenrolled 2000 patients, 557 (28%) of whom had AF before enrollment. Cumulative probability of any sustained or nonsustained WCD-detected VT/VFduring WCD use was significantly higher among patients with a history of AF than without AF (6% vs. 3%, p = .001). Similarly, the recurrent rate of any sustained or nonsustained VT/VFwas significantly higher in patients with prior AF versus no prior AF (131.5 events per 100 patient-years vs. 22.7 events per 100 patient-years, p = .001). Patients with prior AF also had a significantly higher burden of any WCD-detected atrial arrhythmias/SVT/inappropriate arrhythmiastherapy (183.2 events per 100 patient-years vs. 74.8 events per 100 patient-years, p < .001). Our results demonstrate that patients with a history of AF wearing the WCD for risk assessment have a higher incidence of ventricular arrhythmias that may facilitate the decision making for ICD implantation.

Electrophysiological Characterization of Subclinical and Overt Hypertrophic Cardiomyopathy by Magnetic Resonance Imaging-Guided Electrocardiography

BackgroundVentricular arrhythmia in hypertrophic cardiomyopathy (HCM) relates to adverse structural change and genetic status. Cardiovascular magnetic resonance (CMR)–guided electrocardiographic imaging (ECGI) noninvasively maps cardiac structural and electrophysiological (EP) properties. ObjectivesThe purpose of this study was to establish whether in subclinical HCM (genotype [G]+ left ventricular hypertrophy [LVH]−), ECGI detects early EP abnormality, and in overt HCM, whether the EP substrate relates to genetic status (G+/G−LVH+) and structural phenotype. MethodsThis was a prospective 211-participant CMR-ECGI multicenter study of 70 G+LVH−, 104 LVH+ (51 G+/53 G−), and 37 healthy volunteers (HVs). Local activation time (AT), corrected repolarization time, corrected activation-recovery interval, spatial gradients (GAT/GRTc), and signal fractionation were derived from 1,000 epicardial sites per participant. Maximal wall thickness and scar burden were derived from CMR. A support vector machine was built to discriminate G+LVH− from HV and low-risk HCM from those with intermediate/high-risk score or nonsustained ventricular tachycardia. ResultsCompared with HV, subclinical HCM showed mean AT prolongation (P = 0.008) even with normal 12-lead electrocardiograms (ECGs) (P = 0.009), and repolarization was more spatially heterogenous (GRTc: P = 0.005) (23% had normal ECGs). Corrected activation-recovery interval was prolonged in overt vs subclinical HCM (P < 0.001). Mean AT was associated with maximal wall thickness; spatial conduction heterogeneity (GAT) and fractionation were associated with scar (all P < 0.05), and G+LVH+ had more fractionation than G−LVH+ (P = 0.002). The support vector machine discriminated subclinical HCM from HV (10-fold cross-validation accuracy 80% [95% CI: 73%-85%]) and identified patients at higher risk of sudden cardiac death (accuracy 82% [95% CI: 78%-86%]). ConclusionsIn the absence of LVH or 12-lead ECG abnormalities, HCM sarcomere gene mutation carriers express an aberrant EP phenotype detected by ECGI. In overt HCM, abnormalities occur more severely with adverse structural change and positive genetic status.

Do Implantable Cardioverter-Defibrillators Prevent Sudden Cardiac Death in End-Stage Renal Disease Patients on Dialysis?

Chronic kidney disease patients appear to be predisposed to heart rhythm disorders, including atrial fibrillation/atrial flutter, ventricular arrhythmias, and supraventricular tachycardias, which increase the risk of sudden cardiac death. The pathophysiological factors underlying arrhythmia and sudden cardiac death in patients with end-stage renal disease are unique and include timing and frequency of dialysis and dialysate composition, vulnerable myocardium, and acute proarrhythmic factors triggering asystole. The high incidence of sudden cardiac deaths suggests that this population could benefit from implantable cardioverter-defibrillator therapy. The introduction of implantable cardioverter-defibrillators significantly decreased the rate of all-cause mortality; however, the benefits of this therapy among patients with chronic kidney disease remain controversial since the studies provide conflicting results. Electrolyte imbalances in haemodialysis patients may result in ineffective shock therapy or the appearance of non-shockable underlying arrhythmic sudden cardiac death. Moreover, the implantation of such devices is associated with a risk of infections and central venous stenosis. Therefore, in the population of patients with heart failure and severe renal impairment, periprocedural risk and life expectancy must be considered when deciding on potential device implantation. Harmonised management of rhythm disorders and renal disease can potentially minimise risks and improve patients' outcomes and prognosis.

Detection of gene mutation in the prognosis of a patient with arrhythmogenic right ventricular cardiomyopathy: a case report

BackgroundArrhythmogenic right ventricular cardiomyopathy (ARVC), or more recently known as arrhythmogenic cardiomyopathy (ACM), is an heritable disorder of the myocardium characterized by progressive fibrofatty replacement the heart muscle and risk of ventricular arrhythmias and sudden cardiac death (SCD). We report a case study to demonstrate the role of gene mutation detection in risk stratification for primary prevention of SCD in a young patient diagnosed with ARVC.Case presentationA 15-year-old Asian (Vietnamese) male patient with no history of documented tachyarrhythmia or syncope and a family history of potential SCD was admitted due to palpitations. Clinical findings and work-up including cardiac magnetic resonance imaging (MRI) were highly suggestive of ARVC. Gene sequencing was performed for SCD risk stratification, during which PKP2 gene mutation was found. Based on the individualized risk stratification, an ICD was implanted for primary prevention of SCD. At 6 months post ICD implantation, the device detected and successfully delivered an appropriate shock to terminate an episode of potentially fatal ventricular arrhythmia. ICD implantation was therefore proven to be appropriate in this patient.ConclusionsWhile gene mutations are known to be an important factor in the diagnosis of ARVC according to the 2010 Task Force Criteria and recent clinical guidelines, their role in risk stratification of SCD remains controversial. Our case demonstrated that when used with other clinical factors and family history, this information could be helpful in identifying appropriate indication for ICD implantation.

Cardiac MRI in diagnosis, prognosis, and follow-up of hypertrophic cardiomyopathy in children: current perspectives.

Hypertrophic Cardiomyopathy (HCM) is an inherited myocardial disease characterised by left ventricular hypertrophy, which carries an increased risk of life-threatening arrhythmias and sudden cardiac death. The age of presentation and the underlying aetiology have a significant impact on the prognosis and quality of life of children with HCM, as childhood-onset HCM is associated with high mortality risk and poor long-term outcomes. Accurate cardiac assessment and identification of the HCM phenotype are therefore crucial to determine the diagnosis, prognostic stratification, and follow-up. Cardiac magnetic resonance (CMR) is a comprehensive evaluation tool capable of providing information on cardiac morphology and function, flow, perfusion, and tissue characterisation. CMR allows to detect subtle abnormalities in the myocardial composition and characterise the heterogeneous phenotypic expression of HCM. In particular, the detection of the degree and extent of myocardial fibrosis, using late-gadolinium enhanced sequences or parametric mapping, is unique for CMR and is of additional value in the clinical assessment and prognostic stratification of paediatric HCM patients. Additionally, childhood HCM can be progressive over time. The rate, timing, and degree of disease progression vary from one patient to the other, so close cardiac monitoring and serial follow-up throughout the life of the diagnosed patients is of paramount importance. In this review, an update of the use of CMR in childhood HCM is provided, focussing on its clinical role in diagnosis, prognosis, and serial follow-up.

Prognostic value of morphological, biochemical, molecular markers of fibrosis in patients with hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) at the cellular level is characterized by hypertrophy, cardiomyocyte disorganization and myocardial fibrosis areas. The leading death cause in HCM remains sudden cardiac death (SCD). Despite the existing risk scores for SCD in HCM, there are still patients with uncertain SCD risk. In addition, SCD cases are also recorded among low-risk patients. From the above, search for novel markers for a more accurate risk assessment should be continued. Fibrosis is currently suspected to be a substrate of potentially life-threatening ventricular arrhythmias. Despite the increasingly widespread use of cardiac magnetic resonance imaging in the diagnosis of myocardial fibrosis and stratification of patients at high SCD risk, the determination of myocardial fibrosis biomarkers remains a relevant and promising area. The article presents the results of studies proving the diagnostic significance and relationship with the risk of life-threatening cardiac arrhythmias of the following markers: C-propeptide of type I procollagen, matrix metalloproteinase proteins, tissue inhibitor of metalloproteinases 1, microRNA family, soluble suppression of tumorigenicity 2, galectin-3, apelin. Evaluation of these biomarkers can be used to improve risk stratification of patients with HCM.

A paradigm change in sudden cardiac death risk prediction: 'static' goes out, 'dynamic' comes in.

A paradigm change in sudden cardiac death risk prediction: 'static' goes out, 'dynamic' comes in.

Prevalence of prolonged QTc interval among HIV infected patients on highly active antiretroviral therapy (HAART) and its relationship with CD4 cells count and viral load at a tertiary hospital in North Eastern Nigeria.

Patients living with HIV infection remain at increased risk of cardiovascular diseases and sudden cardiac death. Various prevalence of electrocardiographic (ECG) abnormalities among HIV-infected patients were reported: Attamah et al reported the prevalence of electrocardiographic abnormalities among HIV-infected patients as 34.5%, while Orunta et al reported a prevalence of 42.9%, and Njoku et al reported a prevalence of 93.0%. Human immunodeficiency virus-infected patients are at increased risk of developing prolonged QT interval. Sani et al reported the prevalence of prolonged corrected QT interval among HIV-infected patients as 45.0%. Innocent et al reported a prevalence of48.0%, while Ajala et al reported a prevalence of 18%. Prolonged QTc interval increases the risk of premature ventricular contraction which can degenerate into ventricular tachycardia and or ventricular that can result in sudden cardiac death. The study was a cross-sectional conducted among HIV-infected patients receiving HAART at the Federal Medical Centre Nguru, Yobe State, North Eastern Nigeria. One hundred and seven (107) subjects were recruited into the study comprising thirty-three (37.0%) males and 70(65.4%) females. The mean CD4 cell count, and viral load of the studied patients were 612.64±34.75 cells/μL and4646.30±58.68 copies/mL respectively. Twenty (18.7%) patients had prolonged QTc interval, this gave us the prevalence of prolonged QTc in this study as 18.7%. The commonest cardiac rhythm was sinus rhythm (69.2%), followed by sinus tachycardia (26.2%) and atrial fibrillation 5(4.7%). Other electrocardiographic findings include First-degree atrioventricular block was seen in seven (6.5%) patients, Premature ventricular contractions were found in16.8%, RBBB was observed in 2.8%, 3.7% of patients had LBBB and 4.7% had left posterior hemiblock. The distribution of QTc interval according to CD4 cells count and viral revealed a statistically significant difference across the groups. All the patients with prolonged QTc interval had lower CD4 cells count and higher viral load suggesting that HIV disease severity is associated with prolonged QTc interval. In conclusion, the study revealed that the prevalence of prolonged QTc interval among HIV infected patients on highly active antiretroviral therapy was found to be 18.7%, and that HIV disease severity increases the risk of developing prolonged QTc interval.

Case report: A case of an anomalous right coronary artery arising from the left coronary cusp.

Abstract&#x0D; An anomalous origin of the right coronary artery is usually asymptomatic. It is mostly found incidentally on an invasive diagnostic angiogram. It does lead to an increased risk of sudden cardiac death, especially in younger patients. We present a case of a 41-year-old who had presented to the hospital with complaints of chest pain. The patient was evaluated by cardiology who performed an angiography that identified an anomalous origin of the right coronary artery arising from the left coronary cusp but no evidence of coronary artery disease. Once identified, these anomalous vessels should be corrected surgically, as these conditions increase the risk of sudden cardiac death arrhythmia and ischemic events.&#x0D; &#x0D; INTRODUCTION&#x0D; Anomalous aortic origin of the right coronary artery (AAORCA) is an uncommon congenital malformation with varying clinical presentations ranging from asymptomatic to sudden cardiac death (SCD). Those with symptoms or high-risk lesions are usually managed by unroofing or reimplantation, coronary artery bypass graft (CABG), AAORCA treated with right internal memory artery graft with proximal RCA ligation.&#x0D; &#x0D; CASE DESCRIPTION&#x0D; A 41-year-old female patient with obesity and hypertension presented with a 1-year history of intermittent exertional substernal pressure radiating to left shoulder and back. The pain, which lasted about 10 minutes per episode, had been more frequent and intense over the past week.Upon initial evaluation, she was hypertensive at 150/90 mmHg and heart rate 60 bpm. Blood work was unremarkable, including negative serial troponin levels. Electrocardiography showed sinus bradycardia without ischaemic changes. Anomalous origin of RCA was incidentally discovered from computed tomography (CT) of the chest. Coronary angiography and ascending aortography were then performed, which revealed a patent RCA originating from the left coronary cusp (Fig. 1A). CT heart angiography with reconstruction revealed the RCA ostium in the left coronary cusp with a malignant course between the aorta and pulmonary artery and without an obvious intramural segment&#x0D; Discussion:&#x0D; &#x0D; An anomalous origin of the right coronary artery (RCA) is a rare congenital anomaly that was first described in 1948 by White and Edwards. After carrying out angiography in 126,595 patients, Yamanaka and Hobbs reported the incidence of anomalous origin of the right and left coronary arteries as 136 (0.107%) and 22 (0.017%), respectively. The prevalence of an anomalous origin of RCA (ARCA) arising from the left coronary cusp with an inter-arterial course varies between 0.026% and 0.25%. An ARCA is more common than the anomalous origin of the left coronary artery (ALCA), but the latter is shown to be responsible for up to 85% of sudden cardiac deaths (SCD) related to the anomalous origins of arteries. Most coronary anomalies are detected incidentally on diagnostic angiography and are clinically insignificant; some, however, have been associated with an increased risk of SCD. It is second only to hypertrophic cardiomyopathy as a leading cause of SCD in young athletes. Mechanical compression of the RCA by the great vessels, which dilate and compress the RCA during periods of increased stroke volume, is the usual explanation for coronary ischemia. Patients usually have no ischemic changes on an electrocardiogram (ECG) at rest; however, multi-detector computed tomography (MDCT) is being used to evaluate the course of anomalous vessels outlying their relative positions to the aorta and the pulmonary artery. It also gives additional information regarding any stenotic lesion in these anomalous vessels. Echocardiography (Echo), magnetic resonance angiography (MRA), MCDT, and cardiac catheterization are all complementary diagnostic tools for evaluating anomalous coronary arteries [10]. While it is agreed that surgical correction is the standard of care for ALCA, when found, the management for right ARCA is more complicated. Treatment options for these patients include observation with medical therapy, percutaneous intervention (stenting), or surgery. Early diagnosis of coronary artery anomalies based on the patients’ symptoms can help decrease the incidence of sudden cardiac deaths, fatal arrhythmias, and ischemic events in the high-risk population.&#x0D; &#x0D; Conclusions &#x0D; &#x0D; Coronary anomalies should be suspected in symptomatic young patients with a normal cardiac workup. Non-invasive imaging modalities such as a CTCA can help establish the diagnosis

Classification, Diagnosis, and Treatment of Obesity-Related Heart Diseases.

Evidence-based medicine shows that obesity is associated with a wide range of cardiovascular (CV) diseases. Obesity can lead to changes in cardiac structure and function, which can lead to obese cardiomyopathy, subclinical cardiac dysfunction, and even heart failure. It also increases the risk of atrial fibrillation and sudden cardiac death. Many invasive and noninvasive diagnostic methods can detect obesity-related heart disease at an early stage, so that appropriate measures can be selected to prevent adverse CV events. However, studies have shown a protective effect of obesity on clinical outcomes of CV disease, a phenomenon that has been termed the obesity paradox. The "obesity paradox" essentially refers to the fact that the classification of obesity defined by body mass index (BMI) does not consider the impact of obesity heterogeneity on CV disease prognosis, but simply puts subjects with different clinical and biochemical characteristics into the same category. In any case, indicators such as waist-to-hip ratio, ectopic body fat qualitative and quantitative, and CV fitness have been shown to be able to distinguish different CV risks in patients with the same BMI, which is convenient for early intervention in an appropriate way. A multidisciplinary approach, including lifestyle modification, evidence-based generic and novel pharmacotherapy, and surgical intervention, can improve CV outcomes in overweight/obese patients.

Medical Treatment Strategies for Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is a heterogeneous genetic heart disease inherited in an autosomal dominant pattern with an estimated prevalence of 0.6% in the general population. Clinical manifestations of HCM vary considerably, with symptoms ranging from none or mild exercise intolerance to severe lifestyle-limiting symptoms, advanced heart failure, and sudden cardiac death. Current management options for HCM include lifestyle modifications, familial screening with genetic counseling, pharmacotherapy for symptom control, sudden cardiac death risk stratification with or without defibrillator implantation, septal reduction therapy, and, in some cases, heart transplantation. Only recently have strongly targeted medical therapies for HCM, such as myosin inhibitors, been studied in multicenter randomized controlled trials. In this report, we review the currently available medical treatments for HCM and the future directions of HCM pharmacotherapy, and we highlight important unmet needs in this population.