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1.
Cureus ; 16(3): e56462, 2024 Mar.
Article in English | MEDLINE | ID: mdl-38638725

ABSTRACT

Myocardial bridging is an under-recognized cause of angina. This congenital anomaly occurs when a segment of the epicardial coronary artery has a short intra-myocardial course. A significant intra-myocardial course may lead to ischemia, causing anginal symptoms. In this case report, we discuss a rare presentation of myocardial bridging with symptoms of heart failure. The pathology led to a marked degree of ventricular dysfunction and a significant drop in cardiac output (CO), and the patient had severe exertional dyspnea and functional limitations. The ischemic workup with diagnostic imaging and angiograms failed to explain the severity of symptoms, which were only evident in hemodynamic studies and cardiopulmonary exercise testing.

3.
Curr Cardiol Rev ; 15(2): 76-82, 2019.
Article in English | MEDLINE | ID: mdl-30360746

ABSTRACT

Percutaneous mitral valve repair is emerging as a reasonable alternative especially in those with an unfavorable surgical risk profile in the repair of mitral regurgitation. At this time, our understanding of the effects of underlying renal dysfunction on outcomes with percutaneous mitral valve repair and the effects of this procedure itself on renal function is evolving, as more data emerges in this field. The current evidence suggests that the correction of mitral regurgitation via percutaneous mitral valve repair is associated with some degree of improvement in cardiac function, hemodynamics and renal function. The improvement in renal function was more significant for those with greater renal dysfunction at baseline. The presence of Chronic Kidney Disease (CKD) in turn has been associated with poor long-term outcomes including increased mortality and hospitalization among patients who undergo percutaneous mitral valve repair. This was true regardless of the degree of improvement in GFR post repair advanced CKD. The adverse impact of CKD on long-term outcomes was consistent across all studies and was more prominent in those with GFR<30 mL/min/1.73 m². It is clear that from these contrasting evidences of improved renal function post mitral valve repair but poor long-term outcomes including increased mortality in patients with CKD, that proper patient selection for percutaneous mitral valve repair is key. There is a need to have better-standardized criteria for patients who should qualify to have percutaneous mitral valve replacement with Mitraclip. In this new era of percutaneous mitral valve repair, much work needs to be done to optimize long-term patient outcomes.


Subject(s)
Cardiac Surgical Procedures/methods , Heart Valve Prosthesis Implantation/adverse effects , Mitral Valve/physiopathology , Renal Insufficiency, Chronic/complications , Female , Heart Valve Prosthesis Implantation/methods , Hemodynamics , Humans , Male , Treatment Outcome
4.
Curr Cardiol Rev ; 14(3): 192-199, 2018.
Article in English | MEDLINE | ID: mdl-29921207

ABSTRACT

BACKGROUND: Vascular calcification is known to be a strong risk factor for cardiovascular adverse events and mortality. Atherosclerosis, diabetes, aging, abnormal bone mineral homeostasis and high uremic milieu such as chronic kidney disease are major factors that contribute to the progression of vascular calcification. Several mechanisms such as the osteoblastic transition of vascular smooth muscle cells in response to oxidative stress have shed light on the active nature of vascular calcification, which was once thought to be a passive process. The fine interplay of regulatory factors such as PTH, vitamin D3, FGF 23 and klotho reflect the delicate balance between vascular calcification and bone mineralization. Any disturbance affecting this equilibrium of the bonemineral- vascular axis results in accelerated vascular calcification. Bisphosphonates share similar mechanism of action as statins, and hence several studies were undertaken in humans to verify if the benefits proven to be obtained in animal models extended to human models too. This yielded conflicting outcomes which are outlined in this review. This was attributed mainly to inadequate sample size and flaws in the study design. Therefore, this benefit can only be ascertained if studies addressing this are undertaken. CONCLUSION: This review seeks to highlight the pathophysiologic phenomena implicated in vascular and valvular calcification and summarize the literature available regarding the use of bisphosphonates in animal and human models. We also discuss novel treatment approaches for vascular calcification, with emphasis on chronic kidney disease and calciphylaxis.


Subject(s)
Bone and Bones/metabolism , Diphosphonates/chemistry , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Renal Insufficiency, Chronic/metabolism , Vascular Calcification/metabolism , Fibroblast Growth Factor-23 , Humans , Renal Insufficiency, Chronic/drug therapy
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