The subsequent trigger involves a multifactorial susceptibility hit to this anti-angiogenic environment often precipitated by genetic variations in titin (TTN) and troponin C1, slow skeletal and cardiac type (TNNC1) genes, which encode the muscle proteins titin and troponin C, respectively, viral myocarditis, autoimmunity, nutritional deficiencies, hypertension, and an abnormal response to the hyperosmolar stress during pregnancy [29,33,34]. This evidence concerns the gene TTN and viral myocarditis.