Smooth and Cardiac Muscle Physiology

In cardiac muscle, the protein that binds calcium and initiates the interaction between thick and thin filaments is:

Which of the following mechanisms is responsible for the sustained contraction observed in smooth muscle compared to skeletal muscle?

A 52-year-old man from Delhi presents to the emergency department with acute onset chest pain radiating to the left arm and diaphoresis. His blood pressure is 165/95 mmHg, heart rate 102 bpm, and respiratory rate 24/min. ECG shows ST elevation in leads II, III, and aVF. Cardiac troponin I is elevated at 2.8 ng/mL (normal <0.04). Coronary angiography reveals complete occlusion of the right coronary artery. After successful primary PCI and stent placement, the patient's chest pain resolves. However, 48 hours later, he develops progressive dyspnea, orthopnea, and peripheral edema. Echocardiography shows a left ventricular ejection fraction of 32% with global hypokinesis and a dilated left ventricle. Which of the following best explains the cellular mechanism underlying the transition from acute ischemic injury to chronic heart failure in this patient?

A 48-year-old woman from Mumbai presents with a 6-month history of progressive dyspnea on exertion, fatigue, and recurrent syncope. On examination, she has a systolic murmur at the apex, elevated jugular venous pressure, and peripheral edema. Echocardiography reveals a dilated left ventricle (end-diastolic diameter 65 mm), severely reduced ejection fraction (18%), and diffuse hypokinesis. Cardiac MRI shows extensive myocardial fibrosis with a patchy, non-ischemic pattern. Serum troponin is normal. Viral serology and autoimmune markers are negative. Genetic testing reveals a heterozygous mutation in the LMNA gene (lamin A/C). Over the next 3 months, despite optimal medical therapy with ACE inhibitors, β-blockers, and aldosterone antagonists, her ejection fraction declines further to 12%, and she develops recurrent ventricular arrhythmias. Which of the following best explains the cellular basis for the progressive nature of this cardiomyopathy and the arrhythmia susceptibility in LMNA-related disease?