UNASSIGNED: Sudden death accounts for approximately 10% of deaths among working-age adults and is associated with poor air quality. Objectives: To identify high-risk groups and potential modifiers and mediators of risk, we explored previously established associations between fine particulate matter (PM2.5) and sudden death stratified by potential risk factors.
UNASSIGNED: Sudden death victims in Wake County, NC, from 1 March 2013 to 28 February 2015 were identified by screening Emergency Medical Systems reports and adjudicated (n = 399). Daily PM2.5 concentrations for Wake County from the Air Quality Data Mart were linked to event and control periods. Potential modifiers included greenspace metrics, clinical conditions, left ventricular hypertrophy (LVH), and neutrophil-to-lymphocyte ratio (NLR). Using a case-crossover design, conditional logistic regression estimated the OR (95%CI) for sudden death for a 5 μg/m3 increase in PM2.5 with a 1-day lag, adjusted for temperature and humidity, across risk factor strata.
UNASSIGNED: Individuals having LVH or an NLR above 2.5 had PM2.5 associations of greater magnitude than those without [with LVH OR: 1.90 (1.04, 3.50); NLR > 2.5: 1.25 (0.89, 1.76)]. PM2.5 was generally less impactful for individuals living in areas with higher levels of greenspace.
UNASSIGNED: LVH and inflammation may be the final step in the causal pathway whereby poor air quality and traditional risk factors trigger arrhythmia or myocardial ischemia and sudden death. The combination of statistical evidence with clinical knowledge can inform medical providers of underlying risks for their patients generally, while our findings here may help guide interventions to mitigate the incidence of sudden death.

Primary cardiac lymphoma is an exceedingly rare malignant tumor, with diffuse large B-cell lymphoma (DLBCL) being the most prevalent histological subtype. This disease has non-specific clinical manifestations, making early diagnosis crucial. However, DLBCL diagnosis is commonly delayed, and its prognosis is typically poor. Herein, we report the case of a 51-year-old male patient with DLBCL who presented with recurrent chest tightness for 4 months as the primary clinical symptom. The patient was admitted to the hospital and diagnosed with acute myocardial infarction and left ventricular hypertrophy with heart failure. Echocardiography revealed a progression from left ventricular thickening to local pericardial thickening and adhesion in the inferior and lateral walls of the left ventricle. Finally, pathological analysis of myocardial biopsy confirmed the diagnosis of DLBCL. After treatment with the R-CHOP chemotherapy regimen, the patient\'s chest tightness improved, and he was discharged. After 2 months, the patient succumbed to death owing to sudden ventricular tachycardia, ventricular fibrillation, and decreased blood pressure despite rescue efforts. Transthoracic echocardiography is inevitable for the early diagnosis of DLBCL, as it can narrow the differential and guide further investigations and interventions, thereby improving the survival of these patients.

Background In Ghana and other sub-Saharan African countries, hypertension (HTN) prevalence is rapidly increasing. Hypertensive left ventricular hypertrophy (LVH) is associated with excess fibrous tissue deposition throughout the myocardium. This could lead to ventricular arrhythmias and sudden cardiac death. Increased corrected QT dispersion (QTcd) can cause ventricular repolarization and be used to identify patients at risk of ventricular tachyarrhythmia. The measurement of increased QTcd among hypertensive patients is a simple screening tool to stratify patients at cardiovascular risk. Methods A case-control hospital-based study was conducted on 200 consecutive hypertensive patients. Age- and sex-matched control groups of 200 normotensive individuals who gave informed consent were also recruited. The baseline clinical and demographic characteristics of participants were acquired using structured questionnaires. A physical examination and a resting 12-lead ECG were performed. Increased QTcd and LVH were determined. Results The mean age of hypertensive patients was 50.99±6.73 and 48.19±7.17 for the controls (p-value 0.63). The study population was predominantly female (1:2.4 male:female ratio). Higher mean values for QTcd and LVH (Sokolow-Lyon) were observed among hypertensive patients compared to controls. The prevalence of increased QTcd was 45.0% among hypertensive patients compared to 16.5% in controls (χ2 =38.14, p-value <0.0000001, odds ratio = 4.14). Conclusion Increased QTcd is prevalent among hypertensive Ghanaians. Its measurement can be an effective non-invasive screening tool to risk-stratify hypertensive patients.

In the presence of the left ventricle hypertrophy (LVH), the differential diagnosis with hypertrophic cardiomyopathy (HCM) or some phenocopy must be always considered, which can be easily suspected when the hypertrophy is markedly asymmetric. However, when the hypertrophy is homogeneous, especially if the patient has concomitant hypertension, it may be a challenge to distinguish between hypertensive and HCM, although some clinical features may help us to suspect it. In addition, patients with HCM may present with exertional angina due to microcirculation involvement in the setting of the hypertrophy itself or dynamic obstruction in the left ventricular outflow tract, but in some cases, the presence of concomitant coronary artery disease must be suspected as the cause of angina, especially if the patient has an intermediate or high-risk probability of having ischemic heart disease. We present the case of a 46-year-old Afro-American man with poorly controlled hypertension who was found to have severe LVH, and who presented with symptoms of exertional angina during follow-up. We will review the clinical features that can help us in the differential diagnosis in this context.
Ante la presencia de hipertrofia del ventrículo izquierdo (HVI), siempre se debe considerar el diagnóstico diferencial con la miocardiopatía hipertrófica (MCH) o alguna fenocopia, que puede sospecharse fácilmente cuando la hipertrofia es marcadamente asimétrica. Además, los pacientes con MCH pueden presentar angina de esfuerzo debido a la afectación de la microcirculación en el contexto de la propia hipertrofia o si ésta condiciona obstrucción dinámica al tracto de salida del ventrículo izquierdo, pero en algunos casos debe sospecharse la presencia de enfermedad coronaria concomitante como causa de la angina, especialmente si el paciente tiene una probabilidad de riesgo intermedio o alto de padecer cardiopatía isquémica. Presentamos el caso de un varón de 46 años de afroamericana con hipertensión arterial mal controlada a quien se le detectó una HVI severa, y que durante el seguimiento presentó síntomas de angina de esfuerzo. Revisaremos las características clínicas que nos pueden ayudar en el diagnóstico diferencial en este contexto.

UNASSIGNED: Myocardial abnormalities are sometimes overlooked in congenital heart disease (CHD). The co-existence of hypertrophic cardiomyopathy is so uncommon that it is assumed to be a coincidence rather than an association.
UNASSIGNED: A 24-year-old gentleman, who was previously clinically well following a staged Fontan palliation for single-ventricle CHD, was transferred to our centre following an out-of-hospital cardiac arrest. He had return of spontaneous circulation after a period of cardiopulmonary resuscitation. Initial electrocardiogram showed sinus bradycardia. Computed tomography pulmonary angiography ruled out pulmonary embolism. Transthoracic echocardiography and cardiac magnetic resonance (CMR) demonstrated marked ventricular hypertrophy with no left ventricular outflow tract obstruction. Punctate areas of late gadolinium enhancement were noted in the basal septum, and T1 values were consistent with fibrosis. Cardiac catheterization demonstrated low Fontan pressures and normal coronaries. Ventricular tachycardia rapidly degenerating into ventricular fibrillation was induced during electrophysiological studies. Genetic testing demonstrated a pathogenic cardiac myosin-binding protein C variant consistent with co-existent hypertrophic cardiomyopathy. Bisoprolol was initiated and a subcutaneous implantable cardiac defibrillator implanted 4 weeks after his initial presentation. Two years on, he remains well with no therapies from his defibrillator. As well as Fontan surveillance, cascade testing, exercise prescription, and pre-conception counselling were addressed during follow-up.
UNASSIGNED: In CHD, ventricular hypertrophy may relate to congenital or acquired systemic outflow tract obstruction. Contemporary CMR techniques combined with genetic testing can be useful in differentiating between hypertrophy caused by congenital anomaly vs. concurrent cardiomyopathies. Multidisciplinary expertise is critical for accurate diagnosis and optimal care.

UNASSIGNED: Hypertension-induced left ventricular hypertrophy (LVH) is intricately linked to insulin resistance (IR). This research aimed to elucidate the relationship of advanced indices, namely the triglyceride-glucose (TyG) index, the TyG adjusted for body mass index (TyG-BMI), the triglycerides-to-high-density lipoprotein cholesterol ratio (TG/HDL-c), and the metabolic score for IR (METS-IR), with LVH in hypertensive cohorts.
UNASSIGNED: This analytical case-control investigation encompassed 800 individuals aged 18 or above from the Cardiology Department of the Second Affiliated Hospital of Baotou Medical College over a span from January 2021 to April 2022. Data extraction was conducted from inpatient records. The nexus between the four metrics and LVH susceptibility was ascertained via logistic regression models. Furthermore, the receiver operating characteristic (ROC) curve\'s area (AUC) shed light on the discriminative capacities of the distinct IR indicators for LVH, considering other concomitant risk variables.
UNASSIGNED: Post multifaceted covariate adjustments, the fourth quartile figures for TyG-BMI emerged as the most starkly significant (OR: 5.211, 95% CI: 2.861-9.492), succeeded by METS-IR (OR: 4.877, 95% CI: 2.693-8.835). In juxtaposition with other IR-derived indices (TyG and TG/HDL-c), TyG-BMI manifested the paramount AUC (AUC: 0.657; 95% CI: 0.606-0.708). Concurrently, METS-IR exhibited commendable predictive efficacy for LVH (AUC: 0.646; 95% CI: 0.595-0.697).
UNASSIGNED: TyG-BMI and METS-IR displayed superior discriminative capabilities for LVH, underscoring their potential as supplementary indicators in gauging LVH peril in clinical settings and prospective epidemiological research.

A 34-year-old uncontrolled hypertensive male presented with chest pain radiating to the back. Despite severe pain, he was persistently bradycardic at 38 beats per minute. The workup at the emergency department confirmed the presence of an acute Stanford B aortic dissection. Stanford B dissections are not usually associated with bradycardia. It is Stanford A dissections that are mostly linked with bradycardia because Stanford A dissections can cause concomitant coronary artery extension and involvement of the atrioventricular node. This case demonstrates that sinus bradycardia can exist in the acute setting of any painful aortic dissection, even though it might not necessarily involve the coronary arteries.

Cantu syndrome is a rare and complex multisystem disorder characterized by hypertrichosis, facial dysmorphism, osteochondroplasia and cardiac abnormalities. With only 150 cases reported worldwide, Cantu syndrome is now gaining wider recognition due to molecular testing and a growing body of literature that further characterizes the syndrome and some of its most important features. Cardiovascular pathology previously described in the literature include cardiomegaly, pericardial effusion, vascular dilation and tortuosity, and other congenital heart defects. However, cardiovascular involvement is highly variable amongst individuals with Cantu syndrome. In some instances, it can be extensive and severe requiring surgical management and long term follow up.
Herein we report a case of a fourteen-year-old female who presented with worsening pericardial effusion of unknown etiology, and echocardiographic findings of concentric left ventricular hypertrophy, a mildly dilated aortic root and ascending aorta. Her medical history was notable for hemoptysis and an episode of pulmonary hemorrhage secondary to multiple aortopulmonary collaterals that were subsequently embolized in early childhood. She was initially managed with Ibuprofen and Colchicine but continued to worsen, and ultimately required a pericardial window for the management of refractory pericardial effusion. Imaging studies obtained on subsequent visits revealed multiple dilated and tortuous blood vessels in the head, neck, chest, and pelvis. A cardiomyopathy molecular studies panel was sent, and a pathogenic variant was identified in the ABCC9 gene, confirming the molecular diagnosis of autosomal dominant Cantu syndrome.
Vascular anomalies and significant cardiac involvement are often present in Cantu syndrome, however there are currently no established screening recommendations or surveillance protocols in place. The triad of hypertrichosis, facial dysmorphism, and unexplained cardiovascular involvement in any patient should raise suspicion for Cantu syndrome and warrant further investigation. Initial cardiac evaluation and follow up should be indicated in any patient with a clinical and/or molecular diagnosis of Cantu syndrome. Furthermore, whole body imaging should be utilized to evaluate the extent of vascular involvement and dictate long term monitoring and care.

The cardiovascular risk associated with left ventricular hypertrophy (LVH) in the community and, particularly, in the hypertensive fraction of the general population, represents the rationale for its timely and accurate identification in order to implement adequate preventive strategies. Although electrocardiography (ECG) is the first-line and most economical method of diagnosing LVH its accuracy is largely suboptimal. Over the last 70 years, dozens of different ECG criteria, mostly based on measurements of QRS voltages, have been proposed. In this long journey, a few years ago Peguero et al. developed a novel ECG voltage criterion, currently recognized as Peguero-Lo Presti (PLP) suggesting that it has greater sensitivity than traditional ECG-LVH criteria. Considering that in the last 5 years numerous studies have investigated the diagnostic value of this new index, this review aimed to summarize the data published so far on this topic focusing both on the accuracy in identifying the presence of LVH compared with imaging techniques such as echocardiography (ECHO) and magnetic resonance imaging (MRI) and the value in predicting hard outcomes. The evidence in favor of the greater diagnostic accuracy of the PLP criterion in detecting LVH, phenotyped by ECHO or MRI, and in the stratification of hard outcomes compared with traditional ECG criteria does not appear to be sufficiently proven. Given that the diagnosis of LVH by all ECG criteria (including the PLP) exclusively based on the QRS amplitude is largely imprecise, the development of new multiparametric ECG criteria based on artificial intelligence could represent a real improvement in the diagnostic capacity of the ECG.

Fabry disease (FD) is an X-linked, hereditary dysfunction of glycosphingolipid storage caused by mutations in the GLA gene encoding alpha-galactosidase A enzyme. In rare cases, FD may coexist with immunoglobulin A nephropathy (IgAN). We describe a case of concurrent FD, IgAN, and dilated cardiomyopathy-causing mutations in the TTN and BAG3 genes, which has not been reported previously.
A 60-year-old female patient was admitted with a one-week history of facial and lower-limb edema, two-year history of left ventricular hypertrophy and sinus bradycardia, and recurring numbness and pain in three lateral digits with bilateral thenar muscle atrophy. Renal biopsy revealed concurrent FD (confirmed via an alpha-galactosidase A enzyme assay, Lyso-GL-3 quantification, and GLA gene sequencing) and IgAN. Heterozygous mutations in the TTN (c.30,484 C > A;p.P10162T) and BAG3 (c.88 A > G;p.I30V) genes were observed. The patient reported that two of her brothers had undergone kidney transplantation; one died suddenly at 60 years of age, and the other required a cardiac pacemaker. The 35-year-old son of the patient was screened for the GLA gene mutation and found to be positive for the same mutation as the patient. The patient was administered oral losartan (50 mg/day). Enzyme replacement therapy was refused due to financial reasons. Her renal and cardiac functions were stable yet worth closely monitoring during follow-up.
The family history of patients with concurrent heart and renal diseases should be assessed in detail. Genetic testing and histological examinations are essential for diagnosing FD with IgAN.