Ischemic Heart Disease Pathology Study Guide

Ischemic Heart Disease

Ischemic Heart Disease Pathology Video

Ischemic heart disease is a group of syndromes associated with myocardial ischemia.

Ischemic heart disease is the major cause of death in the United States of America (USA).

Ischemic heart disease is typically brought on by coronary artery atherosclerosis, which reduces blood flow to the myocardium.

Risk factors for ischemic heart disease include:

Diet
Cholesterol
Smoking
Age

Angina. Diagram of discomfort caused by coronary artery disease. Pressure, fullness, squeezing or pain in the center of the chest. Can also feel discomfort in the neck, jaw, shoulders, back or arms. Ian Furst. Not altered. CC BY-SA 3.0
Myocardial Infarction. Cross section showing anterior left ventricle wall infarction Patrick J. Lynch. Not altered. CC BY 2.5
Ischemic Heart Disease. Prinzmetal angina Gogradgme. Not altered. CC BY-SA 3.0
Cultivation of mesenchymal stromal cells for clinical treatment. Collagen staining. The cells needs several weeks of proliferation to reach a sufficient number for clinical treatment. The cells are becoming more and more confluent during cultivation and when they are approximately 80–90% confluent (week 5) they are harvested for treatment or for the next expansion passage. Stem cells therapy for cardiovascular repair in ischemic heart disease: How to predict and secure optimal outcome? Kastrup J - The EPMA journal (2011). Not Altered. CC.

Stable Angina

As a result of physical activity or emotional stress, chest pain may occur due to stable angina.

Stable angina is usually the result of atherosclerosis of coronary arteries with less than 70 percent stenosis.

In stable angina, reduced blood flow is not able to meet the metabolic demands of the myocardium during cardiac exertion.

Stable angina represents damage that myocytes can recover from (no necrosis).

Symptoms of stable angina include:

Chest pain with exertion that lasts about 15 minutes
Pain that radiates from the chest to the left arm associated with exertion
Diaphoresis (sweating)
Shortness of breath

Classical electrocardiogram findings of stable angina show ST-segment depression.

The ST-segment depression is due to subendocardial ischemia.

Stable angina is treated by:

Rest
Nitroglycerin

Unstable Angina

Chest pain that occurs with rest is known as unstable angina.

Unstable angina is usually due to rupture of atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery.

Unstable angina represents damage that myocytes can recover from (no necrosis).

Electrocardiogram (ECG) of unstable angina shows ST-segment depression because of subendocardial ischemia.

Unstable angina is relieved by nitroglycerin.

Patients with unstable angina are at increased risk of progression to myocardial infarction.

Unstable Angina. An illustration of a man feeling tightness or pain in the chest - a symptom of angina or of a heart attack. Not altered. CC BY-SA 4.0

Prinzmetal Angina

Prinzmetal angina is episodic chest pain that is not related to exertion.

Prinzmetal angina is due to coronary artery vasospasm.

Prinzmetal angina represents damage that myocytes can recover from (no necrosis).

Electrocardiogram (ECG) of Prinzmetal angina shows ST-segment elevation due to transmural ischemia.

Treatment of Prinzmetal angina includes:

Nitroglycerin
Calcium channel blockers

Ischemic Heart Disease. Prinzmetal angina Gogradgme. Not altered. CC BY-SA 3.0

Myocardial Infarction (MI)

Necrosis of cardiac myocytes occurs in myocardial infarction (MI).

Myocardial infarction (MI) usually occurs due to rupture of an atherosclerotic plaque with thrombosis and complete occlusion coronary artery.

Risk factors of myocardial infarction (MI) include:

Coronary artery vasospasm (due to Prinzmetal angina or cocaine use)
Emboli
Vasculitis (e.g. Kawasaki disease)

Clinical features of myocardial infarction (MI) include:

Sever chest pain that radiates to the left arm
Diaphoresis
Dyspnea

Symptoms of myocardial infarction (MI) are not relieved by nitroglycerin.

The left ventricle (LV) is typically affected by infarction, while the right ventricle (RV) and both atria are typically spared.

The left anterior descending (LAD) artery is the most prevalent involved artery in myocardial infarction (MI) (45 percent of cases).

The right coronary artery (RCA) is the second most prevalent involved artery in myocardial infarction.

Classic cardiac vessel occlusion shows:

Occlusion of left anterior descending artery (LAD) results in infarction of the anterior wall and anterior septum of the left ventricle
Occlusion of the right coronary artery (RCA) results in infarction of the posterior wall, posterior septum, and papillary muscles of the left ventricle
Occlusion of the left circumflex artery results in infarction of the left lateral wall of the left ventricle

The initial phase of myocardial infarction (MI) results in subendocardial necrosis involving less than 50 percent of the myocardial thickness (subendocardial infarction), and the EKG shows ST-segment depression.

Continued or severe ischemia leads to transmural necrosis involving most of the myocardial wall (transmural infarction), and the ECG shows ST-segment elevation.

Laboratory findings of myocardial infarction (MI) show:

Elevated lactate dehydrogenase (LDH) levels
Elevated troponin
Elevated CK-MB

Troponin I is the most sensitive and specific marker (gold standard) for detecting myocardial infarction.

In myocardial infarction, troponin I levels:

Rise 2 – 4 hours after infarction
Peak at 24 hours
Return to normalcy in 7 – 10 days

CK-MB is helpful to detect re-infarction that occurs days after an initial myocardial infarction (MI).

Creatine kinase MB (CK-MB) levels rise four to six hours after infarction, peak at 24 hours, and return to normalcy by 72 hours.

Treatment of myocardial infarction (MI) includes:

MONA BASH

M-Morphine, 2.0 to 4.0 mg IV PRN for severe pain (May repeat dose of 2 to 8 mg at 5 to 15-minute intervals)
O-Oxygen with nasal cannula to keep SaO₂ > 92% to minimize ischemia
N-Nitroglycerin 0.3-0.6 mg SL q5min PRN chest pain (Max: 3 doses within 15 minutes; this is done to vasodilate arteries and promote blood flow)
A-Aspirin in chewable form first 325 mg (chew) if possible, then 81mg QD after that (avoid enteric coated Aspirin; this limits thrombosis)
B-Beta-blocker such as Metoprolol tartrate 25mg po q6h to decrease the physical demand on the heart
A-ACE inhibitor such as Lisinopril 5mg po BID if you are concerned about the patient’s blood pressure to reduce left ventricular dilation
S-Statin that is high intensity such Atorvastatin 80mg po Qbedtime or rosuvastatin 20-40 mg daily
H-Heparin for patients with non-ST elevations, to help anticoagulate them to limit thrombosis

Treatment of a myocardial infarction (MI) may result in a reperfusion injury.

Myocardial Infarction. Areas where pain is experienced in myocardial infarction, showing common (dark red) and less common (light red) areas on the chest and back. J. Heuser - Not altered. CC BY-SA 3.0
Myocardial Infarction. Areas where pain is experienced in myocardial infarction, showing common (dark red) and less common (light red) areas on the chest and back. J. Heuser - not altered. CC BY-SA 3.0
Myocardial Infarction. ECG : AMI with ST elevation in V2-4 Med Chaos - CC BY-SA 4.0
Myocardial Infarction. Cross section showing anterior left ventricle wall infarction Patrick J. Lynch. Not altered. CC BY 2.5
Myocardial Infarction. A 12-lead ECG showing an inferior STEMI due to reduced perfusion through the right coronary artery. Elevation of the ST segment can be seen in leads II, III and aVF. James Heilman, MD - not altered. CC BY-SA 4.0
Myocardial Infarction. human heart. Photo by camilo jimenez.
Examples of myocardial infarctions identified by Late Gadolinium Enhancement imaging in patients with Metabolic Syndrome. Left: Patient with a large, clinically recognized anteroseptal myocardial infarction. Right: Patient with a small, clinically silent subendocardial infarction in the posterolateral wall.Intra-thoracic fat volume is associated with myocardial infarction in patients with metabolic syndrome. Jolly US, Soliman A, McKenzie C, Peters T, Stirrat J, Nevis I, Brymer M, Joy T, Drangova M, White JA - Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance (2013). Not Altered. CC.
Myocardial Infarction. Example of a 76 year old male patient with an acute myocardial infarction (STEMI) of the anterior wall after acute PCI of the occluded LAD with stent implantation (pain-to-balloon time 150 min.). a The water sensitive T2-STIR image demonstrates the edema in the anterior wall (white arrows), c the LGE images demonstrate an almost transmural myocardial infarction (white arrows) with central MVO (asterisk). This indicates almost no myocardial salvage after successful revascularization of the LAD. b shows the T2* image at TE = 15 ms and d the T2* imaging map of the T2* mapping. The central dark area (white arrow) represents pixels with a T2* decay <20 ms indicating postreperfusionhemorrhage. Assessment of acute myocardial infarction: current status and recommendations from the North American society for Cardiovascular Imaging and the European Society of Cardiac Radiology. Stillman AE, Oudkerk M, Bluemke D, Bremerich J, Esteves FP, Garcia EV, Gutberlet M, Hundley WG, Jerosch-Herold M, Kuijpers D, Kwong RK, Nagel E, Lerakis S, Oshinski J, Paul JF, Underwood R, Wintersperger BJ, Rees MR, North American Society of Cardiovascular. ImagingEuropean Society of Cardiac Radiolo - The international journal of cardiovascular imaging (2010). Not Altered. CC.

Reperfusion Injury

Reperfusion of irreversibly damaged myocardial cells leads to calcium influx.

The calcium influx causes hypercontraction of myofibrils (contraction band necrosis).

Return of oxygen and inflammatory cells can result in free radical generation, which further damages myocytes resulting in reperfusion injury.

Sudden Cardiac Death

Sudden cardiac death is the unexpected death because of cardiac disease.

Sudden cardiac death occurs without symptoms or less than 1 hour after symptoms show up.

Sudden cardiac death is typically due to:

Fatal ventricular arrhythmia
Acute ischemia is the most common etiology

Risk factors for sudden cardiac death include:

Atherosclerosis
Mitral valve prolapse
Cardiomyopathy
Cocaine abuse

Ninety percent of patients that die from sudden cardiac death have preexisting severe atherosclerosis.

Sudden Cardiac Death. Atlantic Ocean (Apr. 21, 2004) - Hospital Corpsman 3rd Class Flowers administers chest compressions to a simulated cardiac arrest victim during drills aboard the conventional powered aircraft carrier USS John F. Kennedy (CV 67). Kennedy is completing final Carrier Qualifications (CQ) prior to her upcoming scheduled deployment. U.S. Navy photo by Photographer's Mate Airman Apprentice Nicholas Garrett. (RELEASED) U.S. Navy photo by Photographer's Mate Airman Apprentice Nicholas Garrett. - Not altered. Public Domain
Sudden Cardiac Death. EKG depiction of ventricular fibrillation (no organized rhythm) - Not altered. CC BY-SA 3.0
Post-mortem histopathology with correlating MR image and correlating CT image in two patients with death secondary to primary vascular cause. (A, B and C) Patient 5 with aortic dissection and cardiac tamponade. Aorta showing marked cystic medial degeneration with large pools of acid mucin. Marked disruption of the elastin fibres is noted. Movat pentachrome stain, 10x objective. MR 3-d whole heart image demonstrating severe ascending aortic dilatation, where there is aortic dissection noted posteriorly and there is an associated large haemopericardium. CT image also demonstrating dilated ascending aorta and haemopericardium. The region of dissection is less well identified due to the lower resolution of this scan when compared to the dedicated MR imaging. (D, E and F) Patient 12 with bilateral pulmonary emboli. Occlusive thromboembolism showing early healing by organisation in large pulmonary artery. Movat pentachrome stain, 2x objective. MR 3-d whole heart image demonstrating bilateral pulmonary emboli in the distal branch pulmonary arteries. Note the heterogeneous signal from this region of clot, especially when compared to the more proximal pulmonary arteries, which is more typical of the expected homogenous signal derived from post-mortem related clot. CT showing the branch pulmonary arteries, where clot in the distal RPA is better visualised than in the LPA and the imaging is generally lower resolution than the dedicated MR Imaging.Comparison of conventional autopsy and magnetic resonance imaging in determining the cause of sudden death in the young. Puranik R, Gray B, Lackey H, Yeates L, Parker G, Duflou J, Semsarian C - Journal of cardiovascular magnetic resonance : official journal of the Society for Cardiovascular Magnetic Resonance (2014). Not Altered. CC.
ECGs of two sisters, both of whom experienced sudden cardiac arrest. a ECG recorded only 1 month before sudden cardiac death at the age of 31 years while in bed. b ECG recorded only a few months before resuscitation from IVF at the age of 44 years, while drinking coffee. ECG a, courtesy of Dr. M.P. van den Berg, University Medical Center Groningen, the Netherlands. Founder mutations in the Netherlands: familial idiopathic ventricular fibrillation and DPP6. Postema PG, Christiaans I, Hofman N, Alders M, Koopmann TT, Bezzina CR, Loh P, Zeppenfeld K, Volders PG, Wilde AA - Netherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation (2011). Not Altered. CC.

Chronic Ischemic Heart Disease

Chronic ischemic heart disease results in poor myocardial function because of chronic ischemic damage (with or without infarction).

Chronic ischemic heart disease may progress to congestive heart failure (CHF).

Ischemic Heart Disease. Micrograph of a coronary artery with the most common form of coronary artery disease (atherosclerosis) and marked luminal narrowing. Masson's trichrome. Nephron - Not altered. CC BY-SA 3.0
Myocardial Infarction. Cross section showing anterior left ventricle wall infarction Patrick J. Lynch. Not altered. CC BY 2.5
Ischemic Heart Disease. Prinzmetal angina Gogradgme. Not altered. CC BY-SA 3.0
Angina. Diagram of discomfort caused by coronary artery disease. Pressure, fullness, squeezing or pain in the center of the chest. Can also feel discomfort in the neck, jaw, shoulders, back or arms. Ian Furst. Not altered. CC BY-SA 3.0
Cultivation of mesenchymal stromal cells for clinical treatment. Collagen staining. The cells needs several weeks of proliferation to reach a sufficient number for clinical treatment. The cells are becoming more and more confluent during cultivation and when they are approximately 80–90% confluent (week 5) they are harvested for treatment or for the next expansion passage. Stem cells therapy for cardiovascular repair in ischemic heart disease: How to predict and secure optimal outcome? Kastrup J - The EPMA journal (2011). Not Altered. CC.