Cardiac Contractility Modulation CCM is a brand new therapy that can help salvage heart failure patients with very poor prognosis. Dr. Basu-Ray and his team performed the first case of CCM in region and one of the early cases in the USA.

Chronic Heart failure is a common health problem with over 6.5 million suffering if not more. In the US, the annual direct cost of heart failure (HF) is estimated at over $30 billion, largely driven by the >1 million hospitalizations in which HF is the primary discharge diagnosis. Heart failure is currently treated with a slew of medication called Goal Directed Medical Therapy (GDMT) with many patient not being able to tolerate the medications or fails to improve on them. Approximately one third of these patients depending on the population studies are eligible for device therapy for heart failure commonly called Cardiac Resynchronization Therapy (CRT or BiV in short). Unfortunately CRT works in only 7 out of 10 heart failure patients implanted with it. Patient not responding to either GDMT and CRT (or those not a candidate for CRT) are thus not uncommon and as expected have a very poor prognosis. Untreated heart failure can have worse prognosis than many cancers.

Cardiac contractility modulation (CCM) is a state of art new device-based therapy for heart failure (HF) that involves applying relatively high-voltage (≈7.5 V), long-duration (≈20 milliseconds), biphasic electric signals to the right ventricular septal wall during the absolute myocardial refractory period. Accordingly, CCM signals do not elicit a new contraction; rather, they influence the biology of the failing myocardium. CCM signals have been shown to improve heart failure by improving Ejection Fraction(EF). Three-dimensional echocardiographic studies showed that CCM induces reverse LV remodeling and improves EF over time. CCM exerts a multitude of biochemical and molecular effects locally and remotely from the site of stimulation, including shifts of a large number of abnormally expressed genes toward normal, many of which involve pathways that regulate calcium cycling and myocardial contraction.