Dr Azra Parveen Senior Registrar Medicine. Acute myocardial infarction is the rapid development of myocardial necrosis caused by a critical imbalance.

Slides:



Advertisements
Similar presentations
Muscular System by: Daniel Gable
Advertisements

Biochemical Markers for Diagnosis of Myocardial Infarction.
1 Lecture | Dr. Usman Ghani
Atherosclerosis Mike Clark, M.D.. Terms Arteriosclerosis – hardening of the arteries Atherosclerosis – a form of arteriosclerosis Venosclerosis Arteriolosclerosis.
Pathogenesis of Atherosclerosis Judith Berliner, Ph.D. Departments of Pathology and Medicine Division of Cardiology David Geffen School of Medicine at.
PBL CV 2 Pathophysiology of coronary artery disease.
Isoenzymes and Other Markers Mike Clark, M.D.. Isozymes (also known as isoenzymes) are enzymes that differ in amino acid sequence but catalyze the same.
Acute Coronary Syndromes. Acute Coronary Syndrome Definition: a constellation of symptoms related to obstruction of coronary arteries with chest pain.
DR. ABDULRAHMAN AL-AJLAN MYOCARDIAL INFARCTION. Introduction The heart is a muscular organ whose function is pumping of blood around the body. It consists.
Cardiac Markers byN.X.. Cardiac Markers 1. After the loss of integrity of cardiac myocyte membranes, intracellular macromolecules diffuse into the interstitium.
OnSite Troponin I Rapid Test. Cardiac markers are biomarkers measured to evaluate heart function.biomarkers They are often discussed in the context of.
Lecture 5. Infarction The process by which necrosis results from ischemia is called infarction Ischemic necrosis of myocardial cells is one of the commonest.
Myocardial infarction biomarkers Lecture 5. Cases 1 Middle aged man referred by family doctor to a dermatologist because of extensive yellow papules with.
By : dr. samer zahran. Key words myocardium : heart muscle coronary arteries : three major blood vessels supplying blood and oxygen to the heart muscles.
1 Dr. Zahoor Ali Shaikh. 2 CORONARY ARTERY DISEASE (CAD)  CAD is most common form of heart disease and causes premature death.  In UK, 1 in 3 men and.
Muscle Cells & Muscle Fiber Contractions
Biochemical Markers of Myocardial Infarction
The Muscular System Skeletal muscle consists of numerous muscle cells called Muscle fibers. Muscle fiber terminology and characteristics Sarcolemma = plasma.
Pathophysiology of IHD
Ischaemic Heart Disease (Coronary Artery Disease)
Ischemic Heart Disease CVS3 Hisham Alkhalidi. Ischemic Heart Disease A group of related syndromes resulting from myocardial ischemia.
Ischaemic Heart Disease. Aims and Objectives n Ischaemic heart disease –Definition, manifestations, epidemiology, aetiology, pathophysiology, risk factors.
Muscle Tissue A primary tissue type, divided into: A primary tissue type, divided into: –skeletal muscle –cardiac muscle –smooth muscle.
Atherosclerosis CVS lecture 2 Atherosclerosis Shaesta Naseem.
Amino-Terminal Pro-Brain Natriuretic Peptide, Brain Natriuretic Peptide, and Troponin T for Prediction of Mortality in Acute Heart Failure.
Muscles. Smooth muscle Found in the walls of hollow organs and the blood vessels Lack striations Contain less myosin Cannot generate as much tension as.
Biochemical Markers for Diagnosis of Myocardial Infarction Cardiovascular Block Medical Biochemistry Course Dr. Reem M. Sallam, MD, PhD.
Myocardial Infarction  MI = heart attack  Defined as necrosis of heart muscle resulting from ischemia.  A very significant cause of death worldwide.
David Sadava H. Craig Heller Gordon H. Orians William K. Purves David M. Hillis Biologia.blu C – Il corpo umano Musculoskeletal System.
Biochemical Investigations In Heart Disaeses
Ischemic Heart Disease Dr. Ravi Kant Assistant Professor Department of General Medicine.
Dr.Hesham Rashid, MD PATHOGENIC MECHANISMS OF ATHEROSCLEROSIS
Sensory and Motor Mechanisms – chpt 49-. I. Anatomy & physiology of Muscular system n A. 3 types of muscle tissue –1. skeletal muscle aka striated muscle–
Ischaemic Heart Disease CASE A. CASE A: Mr HA, aged 60 years, was brought in to A&E complaining of chest pain, nausea and a suspected AMI.
Mechanisms of Myocardial Contraction Dr. B. Tuana.
MYOCARDIAL INFARCTION
Biochemical Markers of Myocardial Infarction
Biochemical Markers for Diagnosis of Myocardial Infarction
Molecular Basis of Muscle Contraction Standard 9 h. Students know the cellular and molecular basis of muscle ocntraction,including the roles of actin,
Ischemic Heart Disease CVS3 Hisham Alkhalidi. Ischemic Heart Disease A group of related syndromes resulting from myocardial ischemia.
All Exercise Occurs at the Cellular Level So how does a muscle cell work – allowing us to move during exercise?
Dr. Manal Basyouni Cardiac Markers 1Dr. Manal Basyouni.
 Coronary artery disease (also called CAD) is the most common type of heart disease. It is also the leading cause of death for both men and women in.
순환기질환 - 혈관, 림프관 -.
Myocardial Infarction (MI) Prepared by Miss Fatima Hirzallah RNS, MSN,CNS.
1 Atherosclerosis ISCHEMIC CHEART DISEASE. 2 Atherosclerosis ATHEROSCLEROSIS IS THE CHRONIC DISEASE WITH THE LIPID AND PROTEIN ABNORMAL METABOLISMS, WITH.
How do muscle cells contract ?. What is the structure of a muscle fiber ? The sarcolemma, or plasma membrane contains invaginations called T (transverse)
Is atherosclerosis a metabolic disease?
Biochemical Investigations In Heart Disaeses
Biochemical Markers of Myocardial Infarction
Muscle Fiber Contraction
Biochemistry MI Biomarkers Important. Extra Information.
Cardiac enzymes. 2 – Non enzyme proteins The Troponins
LABORATORY FEATURES OF MYOCARDIAL INFARCTION
Cardiac enzymes 1 – Types, Isoenzymes and structure Lecture NO: 2nd MBBS Dr.Muhammad Ramzan.
Biochemical Markers of Myocardial Infarction
The Structure of Skeletal Muscle
Coronary disease million Cancer Cerebrovascular disease
Coronary Artery Disease 2
Ch 13.6: Blood Vessels 13.7: Athrosclerosis and Cardiac Arrhythmias
Cardiac enzymes and cardiac proteins
Cardiac enzymes. 2 – Non enzyme proteins The Troponins
Arterial wall: structure and function
Figure 2 Adaptive immunity in atherosclerosis
Biochemical Markers of Myocardial Infarction
Cardiac profile test.
Macrophages in the Pathogenesis of Atherosclerosis
Atherosclerosis  Christopher K. Glass, Joseph L. Witztum  Cell 
Presentation transcript:

Dr Azra Parveen Senior Registrar Medicine

Acute myocardial infarction is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium.  It is an irreversible myocardial injury from prolonged ischemia.  Accurate and early diagnosis is important in minimizing cellular damage and, consequently, in obtaining a successful outcome for the patient

 Risk Factors: Hyperlipiemia-LDL Diabetes Hypertension Smoking Obesity

Initiation of atherosclerosis Expression of adhesion molecules that allows the leukocytes to stick to the arterial wall. Early lesion- Fatty streak Upon entry into the arterial wall blood monocytes begin to scavenge lipids and become foam cells.

 Stable atherosclerotic plaque Foam cells release further cytokines and effector molecules that stimulate smooth muscle cell migration from the arterial intima into the media, as well as smooth cell proliferation. Smooth muscle cells together with lipd core and matrix form a stable atherosclerotic plaque that will remain asymptomatic until it becomes large enough to obstruct arterial flow.

 Vulnerable plaque Inflammatory cell infiltrate, smooth muscle cell death through apoptosis and matrix degradation by matrix metalloproteinases generate a plaque with a thin fibrous cap and lipid-rich necrotic core. It is called a vulnerable plaque and it can rupture. Plaque rupture will expose its contents to blood and trigger platelet aggregation and thrombosis. It will result in partial or complete obstruction of the blood vessel leading to ischemia or infarction

Markers of cardiac myocyte necrosis: Myoglobin CK Ck-MB Troponin I & T

 Myoglobin is an iron and oxygen binding protein found in muscle tissue  It is only found in the blood stream when it is released following muscle injury  It is a sensitive marker for mucle injury making it a potential marker for myocardial infarction  However elevated myoglobin has low specificity for the diagnosis of myocardial infarction and therefore is not the preferred test

 Cytoplasmic CK is a dimer, composed of M and/or B subunits, which associate forming CK-MM, CK-MB and CK-BB isoenzymes.  CK-MM is the main isoenzyme found in striated muscle  CK-MB is found mainly in cardiac muscle  CK-BB is the predominant isoenzyme found in brain

Serum total CK activity and CK-MB concentration rise in parallel following myocardial injury, starting to increase 4± 6 h after injury, reaching peak serum concentrations after 12±24 h and returning to baseline after 48±72 h. Serum CK- MB is considerably more specific for myocardial damage than is serum total CK, which may be elevated in many conditions where skeletal muscle is damaged. Consequently, CK should not be used for the diagnosis of myocardial injury unless used in combination with other more specific cardiac markers.

 IM injection  Traumatic damage to skeletal muscle  Hypothermia  Exercise  Intoxication  Dose-related side effect in statin treatment

 CK-MB fraction= CKMB /total CK  Rationale for using CK-MB fraction ◦ CK-MB fraction greater than 2.5% is suggestive of myocardial injury

Troponin is a regulatory complex of 3 protein subunits located on the thin filament of the myocardial contractile apparatus. Its function is the regulation of striated and cardiac muscle contraction. The complex regulates the calcium-modulated interaction between actin and myosin on the thin filament.  Troponin C (18 kd)  Calcium-binding subunit  No cardiac specificity  Troponin I (26.5 kd)  Actomyosin-ATP-inhibiting  subunit  Cardiac-specific form  Troponin T (39 kd)  Anchors troponin complex  to theTropomyosin strand

 In the absence of calcium ions, tropomyosin blocks access to the mysosin binding site of actin. When calcium binds to troponin, the positions of troponin and tropomyosin are altered on the thin filament and myosin then has access to its binding site on actin..  When the calcium level decreases, troponin locks tropomyosin in the blocking position and the thin filament slides back to the resting state.

 Troponin C is the same in all muscle tissues  Troponins I and T have cardiac-specific forms, cTnI and cTnT  cTnI and cTnT remain elevated for 10 to 14 days

Detectable in blood 4-12 h, similar to CKMB Peaks h Remains elevated for days