Degenerative mitral stenosis (DMS) is an important cause of mitral stenosis, developing secondary to severe mitral annular calcification. With the increase in life expectancy and improved access to health care, more patients with DMS are likely to be encountered in developed nations. These patients are generally elderly with multiple comorbidities and often are high-risk candidates for surgery. The mainstay of therapy in DMS patients is medical management with heart rate control and diuretic therapy. Surgical intervention might be delayed until symptoms are severely limiting and cannot be managed by medical therapy. Mitral valve surgery is also challenging in these patients because of the presence of extensive calcification. Hence, there is a need to develop an alternative percutaneous treatment approach for patients with DMS who are otherwise inoperable or at high risk for surgery. In this review, we summarize the available data on the epidemiology of DMS and diagnostic considerations and current treatment strategies for these patients.

Degenerative Mitral Stenosis: Unmet Need for Percutaneous Interventions

Cardiovascular diseases remain the primary cause of death.1 Myocardial infarction (MI), angina, and stroke take >16 million lives every year, but the underlying mechanisms by which these often‐fatal cardiovascular events occur tend to escape attention.2 Atherosclerosis is the underlying pathological inflammatory vascular disease not only responsible for most MIs and strokes, but it accounts for 29% of deaths worldwide.1, 3

Once believed to be a passive process, it is now understood that atherosclerosis takes an active route involving several cell types, with contributions from a multitude of organ systems, molecular mechanisms, and other pathological conditions, including, but not limited to, hypertension, hyperlipidemia, and type 2 diabetes mellitus.1, 3, 4, 5 Atherosclerosis is characterized by the accumulation of lipids, fibrous elements, and inflammatory cells within the vascular wall of medium and large muscular and elastic arteries.1, 3, 6 Atherosclerotic plaque formation leads to intimal thickening and luminal stenosis.1 Reduction of blood flow ensues, leading to ischemia of the brain, heart, and extremities and clinically manifesting as MI, angina, or stroke.

The main features of atherosclerosis are endothelial dysfunction, intimal thickening, inflammation, and vascular calcification (VC).4, 7, 8 These processes are considered a consequence to vascular injury.1 VC is characterized by calcium deposition in the walls of the vasculature.5 Expansion of the calcified lesion leads to thrombus formation and, if significant enough, vascular occlusion. Although the exact mechanisms for VC are unknown, there has been an increase in interest about the role Wingless (Wnt) signaling plays in disease pathogenesis. Briefly, the Wnt signaling pathway is an evolutionarily conserved pathway across kingdom Animalia and plays a crucial role in pattern formation during embryogenesis.9 The Wnt signal transduction pathway plays a crucial role in organ formation in embryonic development, cell proliferation, polarity, migration, and differentiation.10 Thus, deregulated Wnt signaling is associated with many human diseases.11 Therefore, it is justifiable to suggest that research delineating atherogenesis, with focus on the contribution of Wnt signaling in the pathogenesis of atherosclerotic calcification, is warranted.

Atherosclerotic Calcification: Wnt Is the Hint

Characterizing Risks Associated With Mitral Annular Calcification in Mitral Valve Replacement.

Degenerative Mitral Stenosis: From Pathophysiology to Challenging Interventional Treatment.

Chronic kidney disease (CKD) is associated with dyslipidemia, but the role of atherogenic lipid fractions in CKD progression remains unclear. Here we assess whether baseline plasma levels of lipoprotein(a) [Lp(a)] and apolipoprotein C-III (apoC-III), causal cardiovascular (CV) risk factors being studied as therapeutic targets, are associated with decreasing estimated glomerular filtration rate (eGFR) over time. In the Penn Diabetes Heart Study (PDHS), a single-center observational cohort of type 2 diabetes patients without clinical CV disease or pre-existing CKD, we performed linear mixed effects modeling with incremental multivariable analysis to evaluate the effects of baseline plasma Lp(a) and apoC-III on the slope of eGFR over time for subjects with longitudinal data (N = 400). Each two-fold higher plasma Lp(a) level was associated with an additional decline in eGFR by 0.50 mL/min/year in the fully adjusted model (p < 0.001). Baseline Lp(a) levels greater than the atherogenic cut-point of 30 mg/dL were associated with a decline in eGFR by 2.75 mL/min/year compared to 1.01 mL/min/year in subjects with baseline Lp(a) less than 30 mg/dL (p < 0.001). Although each two-fold higher apoC-III level was also associated with statistically significant decline in eGFR over time, as expected the association was attenuated after adjusting for baseline triglycerides, the key lipid intermediary regulated by apoC-III in circulation. Elevated baseline plasma Lp(a) levels are associated with a decrease in eGFR over time independent of race, lipid medication use, and albuminuria, whereas elevated baseline apoC-III levels are associated with eGFR decline in a triglyceride-dependent fashion.

/pdf/relation-of-atherogenic-lipoproteins-with-estimated-4fpr3yfyhz.pdf

Relation of atherogenic lipoproteins with estimated glomerular filtration rate decline: a longitudinal study

Cardiovascular risk factors and mitral annular calcification in type 2 diabetes.

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Cardiovascular risk factors and mitral annular calcification in type 2 diabetes.