Mohamad Wahoud

The World Health Organization (WHO) refers to obesity as abnormal or excessive fat accumulation that presents a health risk. Obesity was first designated as a disease in 2012 and since then the cost and the burden of the disease have witnessed a worrisome increase. Obesity and hypertension are closely interrelated as abdominal obesity interferes with the endocrine and immune systems and carries a greater risk for insulin resistance, diabetes, hypertension, and cardiovascular disease. Many factors are at the interplay between obesity and hypertension. They include hemodynamic alterations, oxidative stress, renal injury, hyperinsulinemia, and insulin resistance, sleep apnea syndrome and the leptin-melanocortin pathway. Genetics, epigenetics, and mitochondrial factors also play a major role. The measurement of blood pressure in obese patients requires an adapted cuff and the search for other secondary causes is necessary at higher thresholds than the general population. Lifestyle modifications such as diet and exercise are often not enough to control obesity, and so far, bariatric surgery constitutes the most reliable method to achieve weight loss. Nonetheless, the emergence of new agents such as Semaglutide and Tirzepatide offers promising alternatives. Finally, several molecular pathways are actively being explored, and they should significantly extend the treatment options available.

Introduction: Interatrial block (IAB) from disruption of conduction through Bachmann’s bundle results in atrial electromechanical dysfunction. Delay in conduction and alteration in the pattern of atrial activation causes P-wave lengthening (≥120 ms) and characteristic biphasic P-waves in the inferior ECG leads. IAB has been associated with atrial arrhythmia and risk of stroke. Generally, the anatomic substrate for IAB is a fibrotic atrial myopathy; however, intertrial masses have also been associated with IAB. Lipomatous hypertrophy of the interatrial septum (LHIS) constitutes an anatomical barrier that could similarly lead to IAB. Hypothesis: The presence of LHIS is associated with an increased prevalence of IAB. Methods: A query of the echocardiography database at our institution from 2017 to present revealed 312 subjects with LHIS. Data collection included demographic characteristics, ECG and echocardiographic parameters. Prevalence of IAB and associated clinical variables were assessed. Results: The mean age was 72 years (56% male). In the total group IAB was present in 131 patients (42%). Comparison between the group with IAB versus without IAB was notable for a higher prevalence of stroke in those with IAB (24 subjects versus 16; p value = 0.013). The prevalence of atrial fibrillation was not statistically different between the two groups, but atrial flutter was noted to be more prevalent in those with IAB (16 subjects vs 9; p value = 0.018). Hypertension and male sex were also associated with IAB. Conclusions: Subjects with LHIS have a high prevalence of IAB, likely consequent to localized disruption in conduction through Bachmann’s bundle. We demonstrate a higher prevalence of atrial flutter and stroke in those with LHIS and IAB. These results highlight the importance of LHIS as a potential cause of IAB that can contribute to atrial structural remodeling and electromechanical dysfunction associated with atrial arrhythmia and stroke.

BACKGROUND: Transthoracic echocardiography (TTE) is used to assess aortic stenosis (AS) severity and track disease progression. As the field moves to study medical therapies to halt disease progression, reliable non-invasive imaging markers that are sensitive to small changes in disease progression are needed to enable efficient trial designs. The signal-to-noise ratio of commonly obtained TTE-based measures of progressive (non-severe) AS severity is unknown. METHODS: This is a retrospective study of TTEs done at a tertiary referral centre (Tufts Medical Center, Boston MA). A cohort of patients with progressive AS who had two TTEs done within 30 days (in the absence of valve intervention) and a cohort of progressive AS patients with TTEs ≥ 1 year apart, also without valvular intervention, were assembled. Limits of agreement (LOA) and intraclass correlation (ICC) were calculated for aortic valve area (AVA) by continuity equation, peak velocity, and mean gradient. Cohen's d-statistic (d) was calculated for each hemodynamic assessment and a composite marker to assess sensitivity for detecting disease progression normalised to measurement variability. RESULTS: The reproducibility cohort included 24 patients. The progression cohort included 35 patients. The median age was 70 years (interquartile range [IQR] 13). 22 patients (37.3%) were female. In the progression cohort, the median time between TTEs was 2.2 years (IQR 3.1 years). In the reproducibility cohort, AVA LOA were -0.7 to 0.8, ICC = 0.61; peak velocity LOA were -149.0 to + 126.7, ICC = 0.29; and mean gradient LOA were -16.2 to 12.2, ICC = 0.06. The d-statistic for annualised change in AVA was -0.29, the d-statistic for annualised change in maximum velocity was 0.46, the d-statistic for mean gradient was 0.55. The d-statistic for a composite, including all three hemodynamic markers, was 0.45. CONCLUSIONS: Standard TTE markers of AS severity have variable sensitivity for detecting AS progression. For patients with progressive (non-severe) AS, mean gradient has the highest signal-to-noise ratio and may be the most reliable TTE-based assessment of disease progression.