Cardiac fibrosis may refer to an abnormal thickening of the heart valves due to inappropriate proliferation of cardiac fibroblasts but more commonly refers to the excess deposition of extracellular matrix in the cardiac muscle.
 Fibrotic cardiac muscle is stiffer and less compliant and is seen in the progression to heart failure.
 The description below focuses on a specific mechanism of valvular pathology but there are other causes of valve pathology and fibrosis of the cardiac muscle.
Cardiac muscle (heart muscle) is an involuntary, striated muscle that is found in the walls and histological foundation of the heart, specifically the myocardium.
 Cardiac muscle is one of three major types of muscle, the others being skeletal and smooth muscle.
 These three types of muscle all form in the process of myogenesis.
 The cells that constitute cardiac muscle, called cardiomyocytes or myocardiocytes, predominantly contain only one nucleus, although populations with two to four nuclei do exist.
 The myocardium is the muscle tissue of the heart, and forms a thick middle layer between the outer epicardium layer and the inner endocardium layer.
Intercalated discs are microscopic identifying features of cardiac muscle.
 Cardiac muscle consists of individual heart muscle cells (cardiomyocytes) connected by intercalated discs to work as a single functional organ or syncytium.
 By contrast, skeletal muscle consists of multinucleated muscle fibers and exhibit no intercalated discs.
 Intercalated discs support synchronized contraction of cardiac tissue.
 They occur at the Z line of the sarcomere and can be visualized easily when observing a longitudinal section of the tissue.
Cardiac muscle cells or cardiomyocytes (also known as myocardiocytes or cardiac myocytes) are the muscle cells (myocytes) that make up the cardiac muscle (heart muscle).
 Each myocardial cell contains myofibrils, which are specialized organelles consisting of long chains of sarcomeres, the fundamental contractile units of muscle cells.
 Cardiomyocytes show striations similar to those on skeletal muscle cells.
 Unlike multinucleated skeletal cells, the majority of cardiomyocytes contain only one nucleus, although they may have as many as four.
 Cardiomyocytes have a high mitochondrial density, which allows them to produce adenosine triphosphate (ATP) quickly, making them highly resistant to fatigue.
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle.
 The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.
 Often it is in the center or left side of the chest and lasts for more than a few minutes.
 The discomfort may occasionally feel like heartburn.
 Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat, or feeling tired.
 About 30% of people have atypical symptoms.
 Women more often have atypical symptoms than men.
 Among those over 75 years old, about 5% have had an MI with little or no history of symptoms.
 An MI may cause heart failure, an irregular heartbeat, cardiogenic shock, or cardiac arrest.
Door-to-balloon is a time measurement in emergency cardiac care (ECC), specifically in the treatment of ST segment elevation myocardial infarction (or STEMI).
 The interval starts with the patient's arrival in the emergency department, and ends when a catheter guidewire crosses the culprit lesion in the cardiac cath lab.
 Because of the adage that "time is muscle", meaning that delays in treating a myocardial infarction increase the likelihood and amount of cardiac muscle damage due to localised hypoxia, ACC/AHA guidelines recommend a door-to-balloon interval of no more than 90 minutes.
 Currently fewer than half of STEMI patients receive reperfusion with primary percutaneous coronary intervention within the guideline-recommended timeframe.
 It has become a core quality measure for the Joint Commission on Accreditation of Healthcare Organizations (TJC).
Desmoplakin is a protein in humans that is encoded by the "DSP" gene.
 Desmoplakin is a critical component of desmosome structures in cardiac muscle and epidermal cells, which function to maintain the structural integrity at adjacent cell contacts.
 In cardiac muscle, desmoplakin is localized to intercalated discs which mechanically couple cardiac cells to function in a coordinated syncytial structure.
 Mutations in desmoplakin have been shown to play a role in dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, striate palmoplantar keratoderma, Carvajal syndrome and paraneoplastic pemphigus.
Muhammad Hafizullah (Urdu: محمد حافظ الله‎ ) is a Pakistani professor of cardiology and the current vice chancellor of Khyber Medical University (KMU) in Peshawar.
 He is the project director of the Peshawar Institute of Cardiology and has contributed to national guidelines on thrombolysis, acute coronary syndrome, and ST elevation myocardial infarction developed by the Pakistan Cardiac Society.
Myosin heavy chain, α isoform (MHC-α) is a protein that in humans is encoded by the "MYH6" gene.
 This isoform is distinct from the ventricular/slow myosin heavy chain isoform, MYH7, referred to as MHC-β.
 MHC-α isoform is expressed predominantly in human cardiac atria, exhibiting only minor expression in human cardiac ventricles.
 It is the major protein comprising the cardiac muscle thick filament, and functions in cardiac muscle contraction.
 Mutations in "MYH6" have been associated with late-onset hypertrophic cardiomyopathy, atrial septal defects and sick sinus syndrome.
MYH7 is a gene encoding a myosin heavy chain beta (MHC-β) isoform (slow twitch) expressed primarily in the heart, but also in skeletal muscles (type I fibers).
 This isoform is distinct from the fast isoform of cardiac myosin heavy chain, MYH6, referred to as MHC-α.
 MHC-β is the major protein comprising the thick filament in cardiac muscle and plays a major role in cardiac muscle contraction.

Question: Muhammad Hafizullah has contributed to guidelines on what type of damage to the cardiac muscle?
Answer: Myocardial infarction