Further, a recent study from the Population Health Research Institute, McMaster University and Hamilton Health Sciences, David Braley Research Bldg., Hamilton General Hospital, 237 Barton St. E., Hamilton, ON L8L 2X2, Canada shows that “Rivaroxaban with or without Aspirin in Stable Cardiovascular Disease.” This study was published, in the 27 August 2017 issue of the journal “N Engl J Med.” (the number 1 journal in “Clinical medicine” with an impact factor of 72.406), by Dr. Eikelboom, Stuart J. Connolly and others.
Given that: (1) cardiovascular disease is the leading cause of death worldwide; (2) dilated cardiomyopathy is the leading cause of Heart failure; (3) the raise of death rate, due to cardiovascular disease, has increased from 12.3 million in 1990 to 17.3 million in 2013; (4) 13% of cardiovascular disease occur due to uncontrolled high blood pressure; (5) in India, in 2004, 14.6 lakhs deaths (14% of total deaths) were due to ischemic heart disease; (6) 85% of people over 80 years are susceptible to cardiovascular diseases; (7) the global economic cost spent in the treatment of cardiovascular disease in 2011 was little more than 10 billion US dollars; (8) the death due to cardiovascular disease is higher in low-to-middle income countries compared to developed countries; and (9) an alarming number of people, such as 230 lakhs people, will die from cardiovascular diseases each year by 2030, there is an urgent need to find: (i) a cure to diseases, as mentioned above, leading to cardiovascular disease; (ii) a way to induce regeneration of adult cardiomyocytes that were lost in Myocardial patients; (iii) a cheaper alternative to the existing expensive drugs; and (iv) a side-effect-free Natural product-based drug.
A number of studies suggests that Cardiomyopathy is the result of altered gene expression of contractile proteins. Trbp, an RNA binding protein, has been shown to be required for normal functioning of heart contractions.
Prof Da-Zhi Wang’s research team has shown earlier that inactivation of Trbp in mice leads to progressive cardiomyopathy and heart failure.
This study suggests a combinatorial therapy for Cardiomyopathy. A pharmaceutical mixture encompassing VitaminK1 (Phytonadione/Mephyton) and Asprin (VKASP), by regulating the expression of its target genes, it may: (1) decrease the expression of Sox6; (2) increase the expression of cardiac slow-twitch myofiber proteins; (3) decrease the expression of skeletal fast-twitch myofiber proteins; (4) restore the balance between slow- and fast-twitch myofiber proteins; and (5) alleviate cardiomyopathy (fig. 1).
Figure 1. Mechanistic insights into how a pharmaceutical mixture encompassing VitaminK1 (Phytonadione/Mephyton) and Asprin (VKASP) functions as a cardioprotective agent. VKASP, by increasing the expression of its target genes, it may decrease the expression of Sox6. Thereby, it may increase cardiomyocyte proliferation, augment the number of beating cardiomyocytes, and attenuate cardiomyopathy.
Figure 2. The chemicial structures of VitaminK1 (Phytonadione/Mephyton) and Asprin (VKASP).
Thus, pharmacological formulations encompassing “VitaminK1 (Phytonadione/Mephyton) and Asprin (VKASP)] or their analogues, either alone or in combination with other drugs” may be used to inhibit progressive cardiomyopathy and lethal heart failure.
Given the mechanism of action of VKASP, it may be effectively used to treat and alleviate cardiomyopathy and heart failure.
Undisclosed mechanistic information: How a pharmacological mixture (VKASP) encompassing Vitamin-K1 (VK1) and Asprin (ASP) inhibits the expression of Sox6.