Resolution of dynamic left ventricular outflow tract obstruction and reversible left ventricular hypertrophy in 4 cats.

This case series describes spontaneous resolution of systolic anterior motion of the mitral valve, cessation of a dynamic left ventricular outflow tract obstruction, and reverse cardiac remodeling in 4 young cats. Following initial presentation with or without congestive heart failure, subsequent rechecks documented resolution of systolic anterior motion of the mitral valve and normalization of left heart dimensions. Those cats originally presented with congestive heart failure were successfully weaned off diuretic medications. Atenolol was prescribed to all 4 cats, and all remained on oral atenolol through the final recheck. There was no documented recurrence of progressive heart disease and heart failure in any of the cats. Consideration is given to transient myocardial thickening, spontaneous resolution of mitral valve dysplasia, and response to beta-1 adrenergic antagonism as possible underlying mechanisms. Key clinical message: When presented with young cats with hypertrophic obstructive cardiomyopathy, veterinarians should consider multiple differential diagnoses, as lifespan in these cases may be longer than typically expected for cats with primary hypertrophic cardiomyopathy, even with concurrent congestive heart failure.

Résolution d'une obstruction dynamique de la voie d'éjection du ventricule gauche et d'une hypertrophie réversible du ventricule gauche chez 4 chatsCette série de cas décrit la résolution spontanée du mouvement antérieur systolique de la valve mitrale, la cessation d'une obstruction dynamique de la voie d'éjection du ventricule gauche et le remodelage cardiaque inverse chez 4 jeunes chats. Après une présentation initiale avec ou sans insuffisance cardiaque congestive, des vérifications ultérieures ont documenté la résolution du mouvement antérieur systolique de la valve mitrale et la normalisation des dimensions du cœur gauche. Les chats initialement présentés avec une insuffisance cardiaque congestive ont été sevrés avec succès des médicaments diurétiques. De l'aténolol a été prescrit aux 4 chats, et tous sont restés sous aténolol oral jusqu'au dernier contrôle. Aucune récidive de maladie cardiaque progressive et d'insuffisance cardiaque n'a été documentée chez aucun des chats. L'épaississement transitoire du myocarde, la résolution spontanée de la dysplasie de la valve mitrale et la réponse à l'antagonisme bêta-1 adrénergique sont pris en compte comme mécanismes sous-jacents possibles.Message clinique clé :Lorsqu'ils sont confrontés à de jeunes chats atteints de cardiomyopathie hypertrophique obstructive, les vétérinaires doivent envisager plusieurs diagnostics différentiels, car la durée de vie dans ces cas peut être plus longue que celle généralement attendue pour les chats atteints de cardiomyopathie hypertrophique primaire, même en cas d'insuffisance cardiaque congestive concomitante.(Traduit par Dr Serge Messier).

Role of aldosterone in various target organ damage in patients with hypertensive emergency: a cross-sectional study.

BACKGROUND: Hypertensive emergency is a critical disease that causes multiple organ injuries. Although the renin-angiotensin-aldosterone system (RAS) is enormously activated in this disorder, whether the RAS contributes to the development of the organ damage has not been fully elucidated. This cross-sectional study was conducted to characterize the association between RAS and the organ damage in patients with hypertensive emergencies. METHODS: We enrolled 63 patients who visited our medical center with acute severe hypertension and multiple organ damage between 2012 and 2020. Hypertensive target organ damage was evaluated on admission, including severe kidney impairment (eGFR less than 30 mL/min/1.73 m2, SKI), severe retinopathy, concentric left ventricular hypertrophy (c-LVH), thrombotic microangiopathy (TMA), heart failure with reduced ejection fraction (HFrEF) and cerebrovascular disease. Then, whether each organ injury was associated with blood pressure or a plasma aldosterone concentration was analyzed. RESULTS: Among 63 patients, 31, 37, 43 and 8 cases manifested SKI, severe retinopathy, c-LVH and ischemic stroke, respectively. All populations with the organ injuries except cerebral infarction had higher plasma aldosterone concentrations than the remaining subset but exhibited a variable difference in systolic or diastolic blood pressure. Twenty-two patients had a triad of SKI, severe retinopathy and c-LVH, among whom 5 patients manifested TMA. Furthermore, the number of the damaged organs was correlated with plasma aldosterone levels (Spearman's coefficient = 0.50), with a strong association observed between plasma aldosterone (≥ 250 pg/mL) and 3 or more complications (odds ratio = 9.16 [95%CI: 2.76-30.35]). CONCLUSION: In patients with hypertensive emergencies, a higher aldosterone level not only contributed to the development of the organ damage but also was associated with the number of damaged organs in each patient.

Echocardiographic Findings in Children of Patients Diagnosed with PRKAG2 Syndrome. / Achados Ecocardiográficos em Crianças de Pacientes com Diagnóstico de Síndrome do PRKAG2.

BACKGROUND: PRKAG2 syndrome typically manifests in adolescence and early adulthood, progressing with left ventricular hypertrophy, arrhythmias, and risk of sudden death. Findings of echocardiographic markers before clinical manifestation in children of patients affected by the disease can facilitate prevention strategies and therapeutic planning for this patient group. OBJECTIVE: To identify the existence of echocardiographic findings that manifest early in children of parents affected by PRKAG2 syndrome, while they are still asymptomatic. METHODS: In this cross-sectional observational study, 7 participants who were children of parents with established diagnosis of PRKAG2 syndrome, between the ages of 9 months and 12 years, with proven genetic diagnosis, underwent conventional and advanced echocardiography. Their findings were compared to those of a control group composed of 7 age- and sex-matched volunteers who were healthy from a cardiovascular point of view. P values < 0.05 were considered significant. RESULTS: Conventional echocardiography showed statistically significantly higher values in the case group for left atrium, interventricular septum, left ventricular posterior wall, indexed ventricular mass, and relative wall thickness (p < 0.05). Global longitudinal systolic strain on 2-dimensional echocardiography did not show statistical significance between the case and control groups. None of the parameters on 3-dimensional echocardiography showed statistical significance between groups. CONCLUSION: Children diagnosed with PRKAG2 showed echocardiographic findings indicative of a tendency toward cardiac hypertrophy. Echocardiography can be a useful tool in the evaluation and follow-up of this patient group before the onset of clinical manifestations.

FUNDAMENTO: A síndrome do PRKAG2 tipicamente se manifesta na adolescência e início da idade adulta, cursando com hipertrofia ventricular esquerda, arritmias e risco de morte súbita. O achado de marcadores ecocardiográficos antes da manifestação clínica nos filhos de pais acometidos pela doença pode facilitar a estratégia de prevenção e planejamento terapêutico para esse grupo de pacientes. OBJETIVO: Identificar a existência de achados ecocardiográficos que se manifestem precocemente nos filhos de pais acometidos por síndrome do PRKAG2, enquanto ainda assintomáticos. MÉTODOS: Estudo observacional transversal em que sete participantes, filhos de pais com diagnóstico estabelecido de síndrome do PRKAG2, com idades entre 9 meses e 12 anos e diagnóstico genético comprovado, foram submetidos à ecocardiografia convencional e por técnicas avançadas, tendo seus achados comparados aos de grupo controle composto por sete voluntários pareados por sexo e idade, hígidos do ponto de vista cardiovascular. Um valor de p < 0,05 foi considerado significante. RESULTADOS: A ecocardiografia convencional mostrou valores aumentados com significância estatística no grupo caso para átrio esquerdo, septo interventricular, parede posterior do ventrículo esquerdo, massa ventricular indexada e espessura relativa da parede (p < 0,05). O strain sistólico longitudinal global obtido pelo ecocardiograma bidimensional não mostrou diferença estatisticamente significativa entre os grupos caso e controle. Nenhum dos parâmetros ao ecocardiograma tridimensional apresentou significância estatística entre os grupos. CONCLUSÃO: Crianças diagnosticadas com PRKAG2 demonstraram achados ecocardiográficos indicativos de tendência à hipertrofia cardíaca. A ecocardiografia pode ser uma ferramenta útil na avaliação e seguimento desse grupo de pacientes, antes do início de manifestações clínicas.

When Paying Attention Pays Back: Missense Mutation c.1006G>A p. (Val336Ile) in PRKAG2 Gene Causing Left Ventricular Hypertrophy and Conduction Abnormalities in a Caucasian Patient: Case Report and Literature Review.

PRKAG2 cardiomyopathy is a rare genetic disorder that manifests early in life with an autosomal dominant inheritance pattern. It harbors left ventricular hypertrophy (LVH), ventricular pre-excitation and progressively worsening conduction system defects. Its estimated prevalence among patients with LVH ranges from 0.23 to about 1%, but it is likely an underdiagnosed condition. We report the association of the PRKAG2 missense variant c.1006G>A p. (Val336Ile) with LVH, conduction abnormalities (short PR interval and incomplete right bundle branch bock) and early-onset arterial hypertension (AH) in a 44-year-old Caucasian patient. While cardiac magnetic resonance (CMR) showed a mild hypertrophic phenotype with maximal wall thickness of 17 mm in absence of tissue alterations, the electric phenotype was relevant including brady-tachy syndrome and recurrent syncope. The same variant has been detected in the patient's sister and daughter, with LVH + early-onset AH and electrocardiographic (ECG) alterations + lipothymic episodes, respectively. Paying close attention to the coexistence of LVH and ECG alterations in the proband has been helpful in directing genetic tests to exclude primary cardiomyopathy. Hence, identifying the genetic basis in the patient allowed for familial screening as well as a proper follow-up and therapeutic management of the affected members. A review of the PRKAG2 cardiomyopathy literature is provided alongside the case report.

Predictive value of remnant cholesterol for left ventricular hypertrophy and prognosis in hypertensive patients with heart failure: a prospective study.

BACKGROUND AND AIM: Remnant cholesterol (RC) is substantially related to negative outcomes in cardiac patients. Patients with coexisting hypertension and heart failure (HF) often develop left ventricular hypertrophy (LVH) and have poor prognoses. This study investigated baseline RC levels and LV remodelling and patients' prognoses. METHODS AND RESULTS: Six hundred thirty consecutive individuals with hypertension and HF participated in this prospective trial from October 2018 to August 2020. Based on left ventricular mass index (LVMI), 560 those eligible were separated into LVH and non-LVH groups. Multiple linear regression and receiver operating characteristic (ROC) curves examined the RC and LV relationship. A Cox regression analysis was conducted to examine the predictive value of RC for clinical outcomes. The LVH group presented significantly elevated values of RC, triglyceride, and cholesterol and decreased high-density lipoprotein cholesterol (HDLC). The optimal cutoff value for RC to predict LV remodelling was 0.49. The subjects were observed for a median of 58 months, and 104 participants met the primary endpoint. The risk models involving the two Cox models were adjusted to incorporate confounding factors, which revealed that those with elevated baseline levels of RC were more susceptible to cardiovascular mortality, as shown by an increased hazard ratio. (HR: 1.91, 95% CI: 1.62-2.26 vs. HR: 1.75, 95% CI: 1.43-2.16, P < 0.001). CONCLUSIONS: RC is linked to LV remodelling in patients with hypertensive HF, with LVH having greater RC values. Moreover, patients with hypertensive HF who had a higher RC suffered from an increased risk of cardiovascular mortality. TRIAL REGISTRATION: NCT03727828, 21 Oct 2018.

A Cautionary Tale of Hypertrophic Cardiomyopathy-From "Benign" Left Ventricular Hypertrophy to Stroke, Atrial Fibrillation, and Molecular Genetic Diagnostics: A Case Report and Review of Literature.

This case report concerns a 48-year-old man with a history of ischemic stroke at the age of 41 who reported cardiac hypertrophy, registered in his twenties when explained by increased physical activity. Family history was positive for a mother with permanent atrial fibrillation from her mid-thirties. At the age of 44, he had a first episode of persistent atrial fibrillation, accompanied by left atrial thrombosis while on a direct oral anticoagulant. He presented at our clinic at the age of 45 with another episode of persistent atrial fibrillation and decompensated heart failure. Echocardiography revealed a dilated left atrium, reduced left ventricular ejection fraction, and an asymmetric left ventricular hypertrophy. Cardiac magnetic resonance was positive for a cardiomyopathy with diffuse fibrosis, while slow-flow phenomenon was present on coronary angiography. Genetic testing by whole-exome sequencing revealed three variants in the patient, c.309C > A, p.His103Gln in the ACTC1 gene, c.116T > G, p.Leu39Ter in the PLN gene, and c.5827C > T, p.His1943Tyr in the SCN5A gene, the first two associated with hypertrophic cardiomyopathy and the latter possibly with familial atrial fibrillation. This case illustrates the need for advanced diagnostics in unexplained left ventricular hypertrophy, as hypertrophic cardiomyopathy is often overlooked, leading to potentially debilitating health consequences.

Maternal hemoglobin A1c and left ventricular hypertrophy in infants of mothers with pre-gestational diabetes.

OBJECTIVE: Maternal hemoglobin A1c (HbA1c) has been suggested to be a predictor of left ventricular hypertrophy (LVH) in the offspring of mothers with pre-gestational diabetes mellitus, although there is little data supporting this contention. We aimed to assess the relationship between maternal HbA1c and postnatal LVH. METHODS: We performed a retrospective cohort study of infants born to mothers with pre-gestational diabetes mellitus from 2015 to 2021 at our institution. The primary predictor was maternal HbA1c; neonatal left ventricular mass (LVM) z-score was the primary outcome; LVM z-score was considered as both a continuous variable and a binary variable by dichotomizing at 4 to define LVH. Additionally, we used linear regression to determine the relationship between maternal HbA1c and LVM z-score. RESULTS: There were 116 infants who met inclusion (50% female). Mean maternal HbA1c was generally higher in infants with LVH compared to those without LVH (8.2% with LVH vs. 7.2% without LVH [p = 0.009] in the second trimester, and 7.8% vs. 7.0% [p = 0.025] in the third trimester; no significant difference for first trimester). A greater percentage of infants with LVH were intubated (36% vs. 6%, p < 0.001) and had longer average days of hospitalization (9 vs. 5, p = 0.044). Second and third trimester HbA1c was weakly associated with LVM z-score (R2 = 0.063, p < 0.001 and R2 = 0.068, p < 0.001, respectively); first trimester HbA1c was not significantly predictive of LVM z-score. CONCLUSION: Second and third trimester HbA1c is modestly predictive of LVH in infants born to mothers with pre-gestational diabetes mellitus.

Disordered Gut Microbiome and Alterations in Metabolic Patterns Are Associated With Hypertensive Left Ventricular Hypertrophy.

BACKGROUND: Left ventricular hypertrophy (LVH) is most common when driven by hypertension, and it is a strong independent risk factor for adverse cardiovascular events and death. Some animal models support a role for gut microbiota and metabolites in the development of LVH, but cohort studies confirming these findings in populations are lacking. METHODS AND RESULTS: We investigated the alterations of gut microbiota and metabolites in 30 patients with hypertension, 30 patients with hypertensive LVH, and 30 matched controls on the basis of 16S rDNA and metabolomic analyses. Thirty stool and 90 serum samples were collected in fasting conditions. ANOVA/Kruskal-Wallis/Pearson's χ2/Fisher's exact test and Bonferroni's correction were used (P<0.0167) for comparison among the 3 groups. A regression analysis and subgroup analysis were performed between gut microbiota and left ventricular mass index (LVMI) and metabolites and LVMI, respectively. Spearman correlation analysis was performed between metabolites and flora and metabolites and LVMI. We observed LVH-enriched Faecalitalea (ß=6758.55 [95% CI, 2080.92-11436.18]; P=0.009), Turicibacter (ß=8424.76 [95% CI, 2494.05-14355.47]; P=0.01), Ruminococcus torques group (ß=840.88 [95% CI, 223.1-1458.67]; P=0.013), and Erysipelotrichaceae UCG-003 (ß=856.37 [95% CI, 182.76-1529.98]; P=0.019) were positively correlated with LVMI. A total of 1141 (in sera) and 2657 (in feces) metabolites were identified. There was a sex-specific association between metabolites and LVMI. Significant changes in metabolic pathways in LVH were also observed, especially bile acid and lipid metabolism pathways. CONCLUSIONS: Our study demonstrated the disordered gut microbiota and microbial metabolite profiles in LVH. This highlights the roles of gut bacteria and metabolite in this disease and could lead to new intervention, diagnostic, or management paradigms for LVH. REGISTRATION: URL: https://www.chictr.org.cn; Unique Identifier: ChiCTR2200055603.

Family History of Hypertension and Echocardiographic Left Ventricular Hypertrophy in Hypertensive Nigerians.

Introduction: Studies on the relationship between a family history of hypertension and left ventricular hypertrophy are sparse. We evaluated this relationship in patients with essential hypertension. Methods: A total of 1668 patients with essential hypertension were consecutively enrolled in the prospective Federal Medical Centre Abuja Hypertension Registry. First-degree family history was defined by the presence of a known history of hypertension in any or both parents, siblings, and children. Echocardiographic left ventricular hypertrophy was diagnosed using the criteria of the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Results: The prevalence of a family history of hypertension, echocardiographic, and electrocardiographic left ventricular hypertrophy were 61.7%, 46.8%, and 30.8%, respectively. After multivariable adjustment, paternal history of hypertension [OR: 1.56, CI: 1.20-2.05, p=0.001] was associated with an increased risk of echocardiographic left ventricular hypertrophy, while maternal history of hypertension [OR: 0.72, CI 0.58-0.91, p=0.006] was associated with a reduced risk. Age ≥50 years (p=0.026), duration of hypertension ≥1 year (p=0.047), and heart failure (p < 0.001) were associated with an increased risk of left ventricular hypertrophy, while male sex (p < 0.001) was associated with a reduced risk. Conclusion: Our study showed that a paternal history of hypertension is associated with an increased left ventricular hypertrophy risk among patients with essential hypertension, while maternal history is protective.

Mas receptor blockade impairs exercise-induced cardiac hypertrophy.

Exercise training leads to physiological cardiac hypertrophy and the protective axis of the renin-angiotensin system composed of angiotensin-converting enzyme 2, angiotensin-(1-7), and Mas receptor seems involved in this process. However, the role of the basal activity of the Mas receptor in exercise-induced physiological cardiac hypertrophy is still unclear. We evaluated the effects of the Mas receptor blockade on the left ventricular structure and function of rats submitted to running training. Rats were assigned to 4 groups: sedentary (S), sedentary + A-779 (Mas receptor antagonist, 120 µg/kg/day, i.p.; SA), trained (60-minute treadmill running sessions, five days a week, 8 weeks; T), and trained + A-779 (TA). Systolic blood pressure was higher in sedentary and trained rats treated with A-779 at the end of the experimental period. The A-779 treatment prevented the left ventricular hypertrophy evoked by physical exercise and increased collagen deposition in sedentary and trained rats. Cardiomyocytes from the SA group presented increased length and thickness of the sarcomeres, elongated mitochondria, glycogen deposits, and enlarged cisterns of the sarcoplasmic reticulum. TA group presented a reduced sarcomere thickness and cytoplasm with a degenerative aspect. These findings show that the basal activity of the Mas receptor is essential for the proper turnover of the extracellular matrix in the myocardium and the maintenance of the sarcomeric structure of cardiomyocytes.

Left Ventricular Geometric Pattern Impacts QT Dispersion in Males Athletes and Sedentary Men.

AIM: To (1) compare QT dispersion (QTd) and echocardiographic features between athletes with concentric left ventricular (LV) hypertrophy, athletes with eccentric LV hypertrophy, and sedentary controls with a normal LV geometric pattern and (2) quantify associations between QTd and echocardiographic features within these groups. METHODS: Male athletes competing in different sports and sedentary men were stratified into groups according to their LV geometric pattern. These groups included eccentric LV hypertrophy (LV index > 115 g/m2, relative wall thickness [RWT] < 0.42) consisting of 38 athletes, concentric LV hypertrophy (LV index > 115 g/m2, RWT > 0.42) consisting of 40 athletes, and normal LV geometric pattern (LV index < 115 g/m2, RWT < 0.42) consisting of 40 sedentary controls. Following a cross-sectional design, participants underwent electrocardiographic (ECG) and echocardiographic screening. Data were compared between groups using one-way analyses of variance with Bonferroni post hoc tests. Associations between corrected QTd and echocardiographic variables were quantified using Pearson correlations. RESULTS: Alongside structural disparities between groups, corrected QTd was significantly (p < 0.001) lower in athletes with eccentric LV hypertrophy compared to athletes with concentric LV hypertrophy and sedentary controls. Significant, moderate-to-very-large correlations were found between corrected QTd and interventricular septal wall thickness in athletes with concentric (r = 0.416, p = 0.008) or eccentric LV hypertrophy (r = 0.734, p < 0.001), and sedentary controls (r = 0.464, p = 0.003). CONCLUSION: The provided comparative and relationship data may inform the development of more precise approaches for ECG and echocardiographic screening in athletes, particularly in those with concentric LV hypertrophy who may be at greater risk for developing prolonged QTd.

Progress in diagnosis and treatment of hypertension combined with left ventricular hypertrophy.

BACKGROUND: Hypertension, a worldwide cardiovascular issue, is known to result in significant damage to the left ventricle. Left ventricular hypertrophy refers to an increase in ventricular mass, which is not only the primary independent risk factor for cardiovascular disease onset but also independently related to the risk of death. OBJECTIVES: We sought to synthesize the existing literature on the occurrence and correlation between hypertension and left ventricular hypertrophy and the progress. METHODS: A scoping review was performed based on the methodological framework developed by Arksey & O'Malley. Search in the Pubmed database with no language restrictions, as of September 1, 2024. RESULTS: Of the 8110 articles retrieved, 110 were finally included. The selected articles were published between 1987 and 2024, with 55.5% (61/110) of the studies in the last five years and 14.5% (16/110) of 2024. The studies covered diagnosis, epidemiology, pathophysiology, prognosis, and treatment of hypertension with left ventricular hypertrophy. CONCLUSION: The literature reviewed suggests that studies on hypertension combined with left ventricular hypertrophy covered a variety of clinical progress, especially the clinical trial results of some new drugs that may bring great hope for treatment.

Continuous development of 3D echocardiographic technology may provide more accurate measurements; however, studies with the aim of establishing standard reference values remain in exploratory stages.The field of metabolomics offers a promising approach for studying biomarkers by detecting changes in metabolites associated with physiological or pathological processes induced by diseases. This avenue of research holds potential for the early diagnosis and assessment of LVH.Sodium-glucose co-transporter 2 (SGLT2) inhibitors and metformin are initially indicated for conditions other than left ventricular hypertrophy (LVH); however, emerging evidence suggests that these medications may possess potential clinical value in reversing LVH.

The Kv4 potassium channel modulator NS5806 attenuates cardiac hypertrophy in vivo and in vitro.

The compound NS5806 is a Kv4 channel modulator. This study investigated the chronic effects of NS5806 on cardiac hypertrophy induced by transverse aortic constriction (TAC) in mice in vivo and on neonatal rat ventricular cardiomyocyte hypertrophy induced by endothelin-1 (ET-1) in vitro. Four weeks after TAC, NS5806 was administered by gavage for 4 weeks. Echocardiograms revealed pronounced left ventricular (LV) hypertrophy in TAC-treated mice compared with sham mice. NS5806 attenuated LV hypertrophy, as manifested by the restoration of LV wall thickness and weight and the reversal of contractile dysfunction in TAC-treated mice. NS5806 also blunted the TAC-induced increases in the expression of cardiac hypertrophic and fibrotic genes, including ANP, BNP and TGF-ß. Electrophysiological recordings revealed a significant prolongation of action potential duration and QT intervals, accompanied by an increase in susceptibility to ventricular arrhythmias in mice with cardiac hypertrophy. However, NS5806 restored these alterations in electrical parameters and thus reduced the incidence of mouse sudden death. Furthermore, NS5806 abrogated the downregulation of the Kv4 protein in the hypertrophic myocardium but did not influence the reduction in Kv4 mRNA expression. In addition, NS5806 suppressed in vitro cardiomyocyte hypertrophy. The results provide novel insight for further ion channel modulator development as a potential treatment option for cardiac hypertrophy.

Super-response to renal denervation in treatment-resistant essential hypertension.

Renal denervation may be indicated in patients with treatment-resistant essential hypertension to decrease sympathetic nervous activity and optimise blood pressure. We present the case of a woman in her 50s with long-standing essential hypertension, a previous transient ischaemic attack, obesity and a family history of cardiovascular disease, who presented with persistent 24-hour ambulatory hypertension despite ongoing lifestyle modifications and being on five antihypertensive agents with no evidence of an alternative primary aetiology. She had intermittent palpitations and blurring of vision alongside evidence of left ventricular hypertrophy on a CT scan. She underwent renal denervation, following which, not only was she able to cease all antihypertensive therapy but managed to maintain optimised blood pressure with subsequent reversal of left ventricular hypertrophy. Trials have demonstrated modest but inconsistent reductions in blood pressure whereas our case represents a 'super-response' likely due to a higher number of circumferential ablations in comparison to previous studies.

The syndrome of inferior non-infarctional Q-waves due to segmental basal left ventricular hypertrophy.

Non-infarctional Q-waves in general are often recorded in the ECG, and are attributed to anatomical and electrical ECG axis shifts, presence of accessory pathways, pregnancy, HCM, and other HCM-like segmental LV myocardial hypertrophic states, that are currently not fully characterized, as to their nosological nature. The present focused review concerns in particular inferior Q-waves and their association with segmental basal anterior and/or septal LV hypertophies due to HCM, and other not yet fully characterized basal segmental LV hypertophies. Insights from the currently available literature on the topic are reviewed, and varying opinions about the nature of such hypertophic states are discussed, with some suggestions, for what is needed to be done, for their further pathlogenetic characterization.

Sex-specific cardiac remodeling in aged rats after adolescent chronic stress: associations with endocrine and metabolic factors.

BACKGROUND: Cardiovascular disease is a leading cause of death worldwide. Rates of cardiovascular disease vary both across the lifespan and between sexes. While multiple factors, including adverse life experiences, impact the development and progression of cardiovascular disease, the potential interactions of biological sex and stress history on the aged heart are unknown. To this end, we examined sex- and stress-specific impacts on left ventricular hypertrophy (VH) after aging. We hypothesized that early-life chronic stress exposure impacts behavioral and physiologic responses that predict cardiac remodeling in a sex-specific manner. METHODS: Histological analysis was conducted on hearts of male and female rats previously exposed to chronic variable stress during the late adolescent period (postnatal days 43-62). These animals were challenged with a forced swim test and a glucose tolerance test before aging to 15 months and again being challenged. Predictive analyses were then used to isolate factors that relate to cardiac remodeling among these groups. RESULTS: Early-life chronic stress impacted cardiac remodeling in a sex-specific manner. Among rats with a history of chronic stress, females had increased concentric VH. However, there were few associations within the female groups among individual behavioral and physiologic parameters and cardiac remodeling. While males as a group did not have VH after chronic stress, they exhibited multiple individual associations with cardiac susceptibility. Passive coping in young males and active coping in aged males related to VH in a stress history-dependent manner. Moreover, baseline corticosterone positively correlated with VH in unstressed males, while chronically-stressed males had positive correlations between VH and visceral adiposity. CONCLUSIONS: These results indicate that females as a group are uniquely susceptible to the effects of early-life stress on cardiac remodeling later in life. Conversely, males have more individual differences in vulnerability, where susceptibility to cardiac remodeling relates to endocrine, metabolic, and behavioral measures depending on stress history. These results ultimately support a framework for assessing cardiovascular risk based on biological sex and prior adverse experiences.

Cardiovascular disease is the leading cause of death worldwide. Multiple factors influence the incidence and severity of cardiovascular disease including adverse life experiences, biological sex, and age. Alterations of heart structure predict negative cardiovascular health by impacting blood circulation; however, the potential interactions of stress history and biological sex on the aged heart are unknown. In this study, we examined how chronic stress exposure impacts heart structure in male and female rats after aging. Adolescent male and female rats were chronically stressed and then acutely challenged to examine behavioral, endocrine, and metabolic parameters both immediately following chronic stress and after aging. Heart morphology was quantified to examine how behavioral and physiological responses related to cardiac remodeling. Our results indicate that, as a group, female rats previously exposed to chronic stress were uniquely susceptible to inward remodeling of the heart. Subjects were further divided into sub-groups based on the level of inward remodeling of the ventricle. While male rats did not exhibit group effects on heart structure, individual variability in male heart morphology related to endocrine and metabolic parameters in a stress history-dependent manner. Here, there were interactions with multiple systems including coping behavior, stress hormones, and body composition. Moreover, males without a prior history of chronic stress had correlations between stress hormones and the degree of heart remodeling. However, males that were exposed to chronic stress had correlations between heart structure and abdominal fat. Overall, our results indicate that biological sex and stress history interact to predict cardiovascular susceptibility.

Differentiating Left Ventricular Remodeling in Aortic Stenosis From Systemic Hypertension.

BACKGROUND: Left ventricular (LV) hypertrophy occurs in both aortic stenosis (AS) and systemic hypertension (HTN) in response to wall stress. However, differentiation of hypertrophy due to these 2 etiologies is lacking. The aim was to study the 3-dimensional geometric remodeling pattern in severe AS pre- and postsurgical aortic valve replacement and to compare with HTN and healthy controls. METHODS: Ninety-one subjects (36 severe AS, 19 HTN, and 36 healthy controls) underwent cine cardiac magnetic resonance. Cardiac magnetic resonance was repeated 8 months post-aortic valve replacement (n=18). Principal component analysis was performed on the 3-dimensional meshes reconstructed from 109 cardiac magnetic resonance scans of 91 subjects at end-diastole. Principal component analysis modes were compared across experimental groups together with conventional metrics of shape, strain, and scar. RESULTS: A unique AS signature was identified by wall thickness linked to a LV left-right axis shift and a decrease in short-axis eccentricity. HTN was uniquely linked to increased septal thickness. Combining these 3 features had good discriminative ability between AS and HTN (area under the curve, 0.792). The LV left-right axis shift was not reversible post-aortic valve replacement, did not associate with strain, age, or sex, and was predictive of postoperative LV mass regression (R2=0.339, P=0.014). CONCLUSIONS: Unique remodeling signatures might differentiate the etiology of LV hypertrophy. Preliminary findings suggest that LV axis shift is characteristic in AS, is not reversible post-aortic valve replacement, predicts mass regression, and may be interpreted to be an adaptive mechanism.

Echocardiographic Strain Abnormalities Precede Left Ventricular Hypertrophy Development in Hypertrophic Cardiomyopathy Mutation Carriers.

Hypertrophic cardiomyopathy (HCM) is a genetic disease characterized by unexplained left ventricular hypertrophy (LVH), diastolic dysfunction, and increased sudden-death risk. Early detection of the phenotypic expression of the disease in genetic carriers without LVH (Gen+/Phen-) is crucial for emerging therapies. This clinical study aims to identify echocardiographic predictors of phenotypic development in Gen+/Phen-. Sixteen Gen+/Phen- (one subject with troponin T, six with myosin heavy chain-7, and nine with myosin-binding protein C3 mutations), represented the study population. At first and last visit we performed comprehensive 2D speckle-tracking strain echocardiography. During a follow-up of 8 ± 5 years, five carriers developed LVH (LVH+). At baseline, these patients were older than those who did not develop LVH (LVH-) (30 ± 8 vs. 15 ± 8 years, p = 0.005). LVH+ had reduced peak global strain rate during the isovolumic relaxation period (SRIVR) (0.28 ± 0.05 vs. 0.40 ± 0.11 1/s, p = 0.048) and lower global longitudinal strain (GLS) (-19.8 ± 0.4 vs. -22.3 ± 1.1%; p < 0.0001) than LVH- at baseline. SRIVR and GLS were not correlated with age (overall, p > 0.08). This is the first HCM study investigating subjects before they manifest clinically significant or relevant disease burden or symptomatology, comparing at baseline HCM Gen+/Phen- subjects who will develop LVH with those who will not. Furthermore, we identified highly sensitive, easily obtainable, age- and load-independent echocardiographic predictors of phenotype development in HCM gene carriers who may undergo early preventive treatment.

Effects of concurrent training and N-acetylcysteine supplementation on cardiac remodeling and oxidative stress in middle-aged spontaneously hypertensive rats.

BACKGROUND: This study evaluated the effects of concurrent isolated training (T) or training combined with the antioxidant N-acetylcysteine (NAC) on cardiac remodeling and oxidative stress in spontaneously hypertensive rats (SHR). METHODS: Six-month-old male SHR were divided into sedentary (S, n = 12), concurrent training (T, n = 13), sedentary supplemented with NAC (SNAC, n = 13), and concurrent training with NAC supplementation (TNAC, n = 14) groups. T and TNAC rats were trained three times a week on a treadmill and ladder; NAC supplemented groups received 120 mg/kg/day NAC in rat chow for eight weeks. Myocardial antioxidant enzyme activity and lipid hydroperoxide concentration were assessed by spectrophotometry. Gene expression of NADPH oxidase subunits Nox2, Nox4, p22 phox, and p47 phox was evaluated by real time RT-PCR. Statistical analysis was performed using ANOVA and Bonferroni or Kruskal-Wallis and Dunn. RESULTS: Echocardiogram showed concentric remodeling in TNAC, characterized by increased relative wall thickness (S 0.40 ± 0.04; T 0.39 ± 0.03; SNAC 0.40 ± 0.04; TNAC 0.43 ± 0.04 *; * p < 0.05 vs T and SNAC) and diastolic posterior wall thickness (S 1.50 ± 0.12; T 1.52 ± 0.10; SNAC 1.56 ± 0.12; TNAC 1.62 ± 0.14 * mm; * p < 0.05 vs T), with improved contractile function (posterior wall shortening velocity: S 39.4 ± 5.01; T 36.4 ± 2.96; SNAC 39.7 ± 3.44; TNAC 41.6 ± 3.57 * mm/s; * p < 0.05 vs T). Myocardial lipid hydroperoxide concentration was lower in NAC treated groups (S 210 ± 48; T 182 ± 43; SNAC 159 ± 33 *; TNAC 110 ± 23 *# nmol/g tissue; * p < 0.05 vs S, # p < 0.05 vs T and SNAC). Nox 2 and p22 phox expression was higher and p47 phox lower in T than S [S 1.37 (0.66-1.66); T 0.78 (0.61-1.04) *; SNAC 1.07 (1.01-1.38); TNAC 1.06 (1.01-1.15) arbitrary units; * p < 0.05 vs S]. NADPH oxidase subunits did not differ between TNAC, SNAC, and S groups. CONCLUSION: N-acetylcysteine supplementation alone reduces oxidative stress in untreated spontaneously hypertensive rats. The combination of N-acetylcysteine and concurrent exercise further decreases oxidative stress. However, the lower oxidative stress does not translate into improved cardiac remodeling and function in untreated spontaneously hypertensive rats.

Independent risk factors of left ventricular hypertrophy in non-diabetic individuals in Sierra Leone - a cross-sectional study.

BACKGROUND: Left ventricular hypertrophy (LVH) is a critical factor in heart failure and cardiovascular event-related mortality. While the prevalence of LVH in diabetic patients is well-documented, its occurrence and risk factors in non-diabetic populations remain largely unexplored. This study addresses this issue by investigating the independent risk factors of LVH in non-diabetic individuals. METHODS: This cross-sectional study, conducted meticulously, utilized data from a robust and comprehensive source, DATADRYAD, in the Sierra Leone database, collected between October 2019 and October 2021, including LVH and various variables. All variables were described and screened using univariate analysis, Spearman correlation, and principal component analysis (PCA). The lipid profile, including total cholesterols (TC), triglycerides (TG), high-density lipoprotein (HDL-C), non-high-density lipoprotein (Non-HDL-C), and low-density lipoprotein cholesterol (LDL-C), TC/HDL-C ratio, TG/HDL-C ratio, Non-HDL-C /HDL-C ratio and LDL-C/HDL-C ratio, which quartiles were treated as categorical variables, with the lowest quartile serving as the reference category. Three adjusted models were constructed to mitigate the influence of other variables. To ensure the robustness of the model, receiver operating characteristic (ROC) curves were used to calculate the cutoff values by analyzing the ROC curves. A sensitivity analysis was performed to validate the findings further. RESULTS: The dataset encompasses information from 2092 individuals. After adjusting for potential factors that could influence the results, we found that TC (OR = 2.773, 95%CI: 1.805-4.26), Non-HDL-C (OR = 2.74, 95%CI: 1.7723-4.236), TC/HDL-C ratio (OR = 2.237, 95%CI: 1.445-3.463), Non-HDL-C/HDL-C ratio (OR = 2.357, 95%CI: 1.548-3.588), TG/HDL-C ratio (OR = 1.513, 95%CI: 1.02-2.245) acts as independent risk factors of LVH. ROC curve analysis revealed the predictive ability of blood lipids for LVH, with Non-HDL-C exhibiting area under the curve (AUC = 0.6109), followed by TC (AUC = 0.6084). CONCLUSIONS: TC, non-HDL-C, TC/HDL-C ratio, Non-HDL-C/HDL-C ratio, and TG/HDL-C ratio were independent risk factors of LVH in non-diabetic people. Non-HDL-C and TC were found to be essential indicators for predicting the prevalence of LVH.