COVID-19 is a global pandemic that has had a devastating effect on the health and economy of much of human civilization. While the acute impacts of COVID-19 were the initial focus of concern, it is becoming clear that in the wake of COVID-19, many patients are developing chronic symptoms that have been called Long-COVID. Some of the symptoms and signs include those of postural tachycardia syndrome (POTS). Understanding and managing long-COVID POTS will require a significant infusion of health care resources and a significant additional research investment. In this document from the American Autonomic Society, we outline the scope of the problem, and the resources and research needed to properly address the impact of Long-COVID POTS.

Orthostatic intolerance (OI), having difficulty tolerating an upright posture because of symptoms or signs that abate when returned to supine, is common in pediatrics. For example, ∼40% of people faint during their lives, half of whom faint during adolescence, and the peak age for first faint is 15 years. Because of this, we describe the most common forms of OI in pediatrics and distinguish between chronic and acute OI. These common forms of OI include initial orthostatic hypotension (which is a frequently seen benign condition in youngsters), true orthostatic hypotension (both neurogenic and nonneurogenic), vasovagal syncope, and postural tachycardia syndrome. We also describe the influences of chronic bed rest and rapid weight loss as aggravating factors and causes of OI. Presenting signs and symptoms are discussed as well as patient evaluation and testing modalities. Putative causes of OI, such as gravitational and exercise deconditioning, immune-mediated disease, mast cell activation, and central hypovolemia, are described as well as frequent comorbidities, such as joint hypermobility, anxiety, and gastrointestinal issues. The medical management of OI is considered, which includes both nonpharmacologic and pharmacologic approaches. Finally, we discuss the prognosis and long-term implications of OI and indicate future directions for research and patient management.

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Abstract-Our studies have established that a single intracardiac administration of the retroviral vector containing angiotensin II type I receptor antisense gene causes prolonged antihypertensive actions in the spontaneously hypertensive rat. These results suggest that antisense gene therapy is a conceptually valid strategy for the control of hypertension at the genetic level. To evaluate whether attenuation of the pathophysiological aspects of hypertension are dependent on the blood pressure lowering actions of antisense gene therapy, we chose the renin transgenic rat as a hypertensive animal model and cardiac hypertrophy as the hypertension-associated pathophysiology. A single intracardiac administration of the retroviral vector containing angiotensin II type I receptor antisense in the neonatal rat resulted in long-term expression of the antisense transgene in various cardiovascular-relevant tissues, including the heart. This expression was associated with a significant attenuation of cardiac hypertrophy despite its failure to normalize high blood pressure. Developmental studies indicated that cardiac hypertrophy was evident as early as 16 days of age in viral vector-treated control transgenic rats, despite these animals exhibiting normal blood pressure. These observations demonstrate that, in the renin-transgenic rat, the onset of cardiac hypertrophy occurs during development and is prevented without normalization of high blood pressure. Collectively, these results provide further proof of the concept and indicate that antisense gene therapy could successfully target the local tissues' renin-angiotensin system to produce beneficial cardiovascular outcomes. Key Words: antisense elements Ⅲ rat, transgenic Ⅲ renin-angiotensin system Ⅲ hypertension, essential Ⅲ genes L eft ventricular hypertrophy (LVH) is a risk factor for cardiovascular-related mortality. Besides high blood pressure (BP), other hemodynamic factors that affect LVH include increased arterial stiffness, blood viscosity, and volume overload. However, increasing evidence has demonstrated a role for nonhemodynamic factors such as the sympathetic nervous system, the local renin-angiotensin system, aldosterone, and genetic factors in the modulation of BP-independent LVH. [1][2][3][4][5][6][7] Recent clinical and experimental studies have demonstrated that pharmacological agents, such as angiotensin converting enzyme (ACE) inhibitors can reduce LVH independently of a reduction in BP. 8,9 This evidence implicates the role of the tissue-based renin-angiotensin system (RAS) in the development of end-organ damage and demonstrates that the pathophysiology may be independent of high BP. However, it has not been established whether the end-organ damage observed in hypertension is a result of high BP or due to an inherently hyperactive RAS.The renin-transgenic rat (TGR mRen2) has been developed as an animal model of hypertension that exhibits fulminant hypertension and displays cardiac and vascular hypertrophy because of an overexertion of renin in various tiss...

Fenestrated atrial septal defects (F-ASDs) may pose a challenge to device closure; recently, a cribriform device with a minimal connecting intrawaist diameter and large, equal left- and right-sided discs has been designed to cover more than one adjacent defect. This study demonstrates the feasibility and technical aspects of closing F-ASDs using this new device. Sixteen patients between August 2003 and January 2006 were included in this study. The inclusion criterion was the presence of a F-ASD diagnosed by transesophageal echocardiography. One of the three available cribriform ASD device sizes (18, 25, or 35 mm) was implanted. Patients were followed for at least 1 year after the procedure. Thirteen patients had successful cribriform ASD device implantation (median age and weight, 12.5 years and 36 kg, respectively). Ten patients (62%) had an associated atrial septal aneurysm. The mean procedure time was 75.6 +/- 28.5 min and the mean fluoroscopy time 14.8 +/- 6.3 min. The RVEDD was significantly reduced, from a mean of 24.2 mm to 21.0 (p < 0.05). One patient developed atrial tachycardia requiring cardioversion during the procedure. There were no embolic events, heart block, or mortality. Complete closure was 10 of 13 (77 %) the next day and 12 of 13 (92%) at 6 and 12 months. We conclude that the cribriform Amplatzer device can be successfully and safely used in patients with F-ASDs. Complete closure may take up to 6 months.

Cooling during RF ablation of atrial tachycardia clearly yielded greater power delivery in vivo and was associated with success.

This is a retrospective study that includes all patients with fenestrated ASDs who were scheduled for catheter closure between August 2003 and December 2007 in Hamad hospital and University of Cairo. Forty-four patients were diagnosed as having fenestrated ASDs with and without septal aneurysm by transthoracic echocardiography

Transcatheter closure of perimembranous and muscular ventricular septal defects is effective, however, these patients need to be followed up regularly to detect device-related problems, specifically, aortic and tricuspid valve regurgitation.