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Valve Disease
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Supravalvar aortic stenosis is the least common type of left ventricular outflow obstruction (seeFig. 3.29a) and most patients with this condition have Williams syndrome. Williams syndrome is also known as idiopathic infantile hypercalcaemia and patients go on to develop renal calcification. It is a rare multi-system genomic disorder, caused by 7q11.23 microdeletion with a prevalence of 1/7500–1/20 000 live births. Virtually all cases have mental retardation, with characteristic elfin-type faces. There is disordered mosaic architecture in the elastic tissue of the aortic media giving rise to a hypoplastic thickened aorta with congenital supravalvar aortic stenosis. The lesion may be present as a discrete shelf, as a so-called hour-glass deformity or as a tubular variety in which most of the aortic arch and its branches are thickened, which is the rarest. The coronary arteries arise from the segment under high pressure and this causes them to become dilated and tortuous with early onset of atherosclerosis. This, in combination with left ventricular hypertrophy is responsible for sudden deaths in this condition. Mortality is highest in patients with multilevel obstruction.
Testing the master athlete
Published in R. C. Richard Davison, Paul M. Smith, James Hopker, Michael J. Price, Florentina Hettinga, Garry Tew, Lindsay Bottoms, Sport and Exercise Physiology Testing Guidelines: Volume I – Sport Testing, 2022
R. C. Richard Davison, Paul M. Smith
Data from the UK suggest that myocardial disease typically accounts for 40% of SCD in all athletes, being more prevalent in older athletes. The predominant causes were idiopathic left ventricular hypertrophy (LVH) and/or fibrosis and arrhythmogenic right ventricular cardiomyopathy (ARVC) (Finocchiaro et al., 2016). The majority of athletes died during exertion (61%), and only a minority of subjects (8%) had a family history of sudden death. Unfortunately, we do not know the relationship between age and circumstances of death, but many of the fatalities at rest are related to sudden arrhythmic death syndrome (SADS), which is more common in the younger athlete. The older athlete is more likely to die during exercise with coronary artery disease (CAD) as the predominant cause of SCD (Chugh and Weiss, 2015; Finocchiaro et al., 2016). The significantly lower prevalence of arrhythmias in the older population suggests that pre-participation electrocardiogram (ECG) screening may be of limited use although data from Jensen-Urstad et al. (1998) suggest that abnormal arrhythmias are highly prevalent in elderly (>70 yr of age) lifelong strenuous exercisers. Indeed, the European Society of Cardiology updated their ECG screening criteria in 2010 to distinguish training-related and training-unrelated changes (Corrado et al., 2010). Morrison et al. (2016) suggested that while cardiac screening protocols do exist around the world, researchers have not yet systematically and extensively evaluated them, particularly for their suitability for master athletes.
Hypertension
Published in Henry J. Woodford, Essential Geriatrics, 2022
A physical examination may detect signs of end-organ damage, such as hypertensive retinopathy (seeTable 18.1) or signs of left ventricular enlargement. Electrocardiograph (ECG) or chest X-ray tests may provide further evidence of left ventricular hypertrophy. To help assess vascular risk, urine should be tested for proteinuria and haematuria. Blood tests can measure glycated haemoglobin (HbA1C), electrolytes, creatinine, estimated glomerular filtration rate and cholesterol.13
Metformin: evidence from preclinical and clinical studies for potential novel applications in cardiovascular disease
Published in Expert Opinion on Investigational Drugs, 2023
Adel Dihoum, Graham Rena, Ewan R Pearson, Chim C Lang, Ify R Mordi
Left ventricular hypertrophy is a key risk factor for development of heart failure and is associated with an increased risk of adverse cardiovascular outcome [50]. Regression of LVH using antihypertensive therapy is associated with a reduction in adverse cardiovascular events [51,52]. Metformin may reduce cardiac remodeling and hypertrophy via different mechanisms. Metformin reduces myocardial fibrosis and collagen synthesis, which is an important pathophysiological process that increases myocardial stiffness, reducing pumping capacity, and contributes to heart failure [19]. Metformin can inhibit the TGF-β1–Smad3 signaling pathway [53], which plays a critical role in the fibrotic remodeling of the infarcted ventricle [54]. Metformin’s effects on KLF-15 may also play an important role in its effects on LVH [55].
Usefulness of non-gated chest computed tomography scans in the diagnosis of acute myocardial infarction
Published in Baylor University Medical Center Proceedings, 2022
Ahmad Jabri, Laith Alhuneafat, Anas Alameh, Ahmad Al-abdouh, Mohammed Mhanna, Hani Hamade, Farhan Nasser, Adnan Yousaf, Ashish Aneja
A 64-year-old woman with hypertension, hyperlipidemia, and diabetes mellitus type 2 presented to the ED complaining of sudden back pain radiating to her anterior chest for 1 day. Her pain was associated with shortness of breath, nausea, and emesis. The initial electrocardiogram showed ST elevation in precordial lead V1 and a troponin T level of 0.746 µg/mL (normal < 0.10). The patient was given aspirin and nitroglycerin. Chest CT with an aortic dissection protocol was negative for aortic dissection but showed three-vessel CAD with decreased enhancement of the septum/apex (Figure 1a). An echocardiogram showed a left ventricular ejection fraction of 55% with severe hypokinesis of the mid anteroseptal, mid anterior free wall, mid inferior wall, and entire apex. Concentric left ventricular hypertrophy was also present. Right ventricular systolic function was normal. Cardiac catheterization revealed a complete proximal left anterior descending (LAD) artery, which was stented with a drug-eluting stent (Figure 1b).
Anti-hypertensive effects of Callisia fragrans extract on Reno-vascular hypertensive rats
Published in Clinical and Experimental Hypertension, 2022
Xoan Thi Le, Loan Thanh Thi Nguyen, Phuong Thi Nguyen, Tai Van Nguyen, Hiep Van Nguyen, Hang Thi Nguyet Pham, Hong Nguyen Tran, Thang Dac Hoang, Dong Van Le, Kinzo Matsumoto
Administration of C. fragrans extract (500 mg/kg) as well as captopril (20 mg/kg) significantly mitigated the increase in the heart weight, body weight ratio, and left ventricular wall thickness caused in the 2K1C model rats. The prevention of myocardial hypertrophy is one of the major endpoints in the treatment of hypertension since long-term hypertension induces left ventricular hypertrophy, a risk factor for coronary heart disease, congestive heart failure, ventricular arrhythmia, and sudden death (17). Angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and diuretics reportedly reduce the left ventricular mass, whereas alpha-adrenergic blockers and direct-acting vasodilators do not exhibit the effect on myocardial hypertrophy (17). Thus, although the suppressive effect of C. fragans on the left ventricular hypertrophy observed in reno-vascular hypertensive rats was less potent than that of captopril, the present results suggest that C. fragans possesses a beneficial effect on the cardiovascular system besides blood pressure-lowering activity.