Postural orthostatic tachycardia syndrome (POTS) is a clinically heterogeneous disorder with multiple contributing pathophysiologic mechanisms manifesting as symptoms of orthostatic intolerance in the setting of orthostatic tachycardia (increase in heart rate by at least 30 beats per minute upon assuming an upright position) without orthostatic hypotension. The three major pathophysiologic mechanisms include partial autonomic neuropathy, hypovolemia, and hyperadrenergic state. Patients often will exhibit overlapping characteristics from more than one of these mechanisms. The approach to the treatment of POTS centers on treating the underlying pathophysiologic mechanism. Stockings, abdominal binders, and vasoconstrictors are used to enhance venous return in partial neuropathic POTS. Exercise and volume expansion are the main treatment strategies for hypo-volemic POTS. For hyperadrenergic POTS, beta-blockers and avoidance of norepinephrine reuptake inhibitors is important. Attempts should be made to discern which pathophysiologic mechanism(s) may be afflicting patients so that treatment regimens can be individualized.

Cross-clamp time >60 min and concomitant mitral valve surgery were independent predictors of PPM implantation following TVR. Long-term PPM dependency is more prevalent after TVR than other types of valvular surgery.

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The Postural Tachycardia Syndrome (POTS) is the most common disorder seen in autonomic clinics. Cardinal hemodynamic feature of this chronic and debilitating disorder of orthostatic tolerance is an exaggerated orthostatic tachycardia (≥30 bpm increase in HR with standing) in the absence of orthostatic hypotension. There are multiple pathophysiological mechanisms that underlie POTS. Some patients with POTS have evidence of elevated sympathoneural tone. This hyperadrenergic state is likely a driver of the excessive orthostatic tachycardia. Another common pathophysiological mechanism in POTS is a hypovolemic state. Many POTS patients with a hypovolemic state have been found to have a perturbed renin-angiotensin-aldosterone profile. These include inappropriately low plasma renin activity and aldosterone levels with resultant inadequate renal sodium retention. Some POTS patients have also been found to have elevated plasma angiotensin II (Ang-II) levels, with some studies suggesting problems with decreased angiotensin converting enzyme 2 activity and decreased Ang-II degradation. An understanding of these pathophysiological mechanisms in POTS may lead to more rational treatment approaches that derive from these pathophysiological mechanisms.

Oral anticoagulants (OACs) are medications commonly used in patients with atrial fibrillation and other cardiovascular conditions. Both warfarin and direct oral anticoagulants are susceptible to drug-drug interactions (DDIs). DDIs are an important cause of adverse drug reactions and exact a large toll on the health care system. DDI for warfarin mainly involve moderate to strong inhibitors/inducers of cytochrome P450 (CYP) 2C9, which is responsible for the elimination of the more potent S-isomer of warfarin. However, inhibitor/inducers of CYP3A4 and CYP1A2 may also cause DDI with warfarin. Recognition of these precipitating agents along with increased frequency of monitoring when these agents are initiated or discontinued will minimize the impact of warfarin DDI. Direct oral anticoagulants are mainly affected by medications strongly affecting the permeability glycoprotein (P-gp), and to a lesser extent, strong CYP3A4 inhibitors/inducers. Dabigatran and edoxaban are affected by P-gp modulation. Strong inducers of CYP3A4 or P-gp should be avoided in all patients taking direct oral anticoagulant unless previously proven to be otherwise safe. Simultaneous strong CYP3A4 and P-gp inhibitors should be avoided in patients taking apixaban and rivaroxaban. Concomitant antiplatelet/anticoagulant use confers additive risk for bleeding, but their combination is unavoidable in many cases. Minimizing duration of concomitant anticoagulant/antiplatelet therapy as indicated by evidence-based clinical guidelines is the best way to reduce the risk of bleeding.