Browsing by keyword "Editorials"
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C'est LAVi: What Left Atrial Dilatation Tells Us About Diastolic Function in Aortic StenosisCalcific degenerative aortic valve stenosis (AS) is the most common acquired form of heart valve disease that afflicts the elderly population1 and usually comes to attention when an echocardiogram is ordered to evaluate a systolic murmur in an older subject. As is evident to anyone practicing cardiology these days, the advent of transcatheter aortic valve replacement has focused much attention on the evaluation and optimal treatment of patients with AS. AS often has a long latency period in which symptoms are absent, and, importantly, sudden unexpected cardiac death is rare.2,3 With symptom onset, survival is markedly reduced without intervention.4–6 For symptomatic patients with severe AS and normal flow-high gradient characteristics and normal left ventricular ejection fraction (LVEF) (stage D1), aortic valve replacement (AVR) is a class 1 indication. Similarly, for asymptomatic patients with severe AS and LVEF less than fifty percent not because of another cause (stage C2), AVR also is indicated.
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Platelets and Immunity: Going ViralPlatelets are the major blood component bridging immunity and thrombosis. Abundant in the circulation, platelets encounter pathogens at a higher rate than any circulating leukocyte. Viral particles of various blood-borne pathogens such as HIV,1 dengue,2 or even respiratory viruses such as influenza3 are found inside human platelets. Viral infections with these viruses,4 as well as the SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2), can lead to thrombocytopenia5 along with thrombotic complications6–8 in patients. The presence of internalized viral particles, thrombocytopenia, and thrombosis implicates platelets as active participants in immunity during viral infections.
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Serial changes in diastolic function: lessons from the growing field of echo-epidemiologyNormal left ventricular function consists of 2 interrelated processes. Systole comprises a coordinated interplay between fiber shortening, wall thickening, longitudinal shortening, and cardiac twist, which results in the generation of stroke volume. During diastole, which comprises relaxation and untwist, as well as contraction of the atrium, the normal ventricle relaxes and fills to an adequate end-diastolic volume at low pressure—thus optimizing stroke volume in the next systole.1 The noninvasive assessment of systolic and diastolic function is a major undertaking of cardiologists, and in 2015, this assessment is usually performed with echocardiography. The assessment of systolic function, which began with M-mode echocardiography in the 1970s, now comprises both 2D and 3D echocardiography, as well as regional function assessment with speckle tracking. The assessment of diastolic function became routine in the 1980s, with the development of pulsed Doppler measurement of transmitral flow velocities: early (E) and late/atrial contraction (A) velocities and pulmonary venous flows.2