Ischemic Heart Disease: Causes, Symptoms, Diagnosis & Full Management Plan

Ischemic Heart Disease Symptoms

Question. Write clinical features, risk factors, diagnosis, and management of ischemic heart disease.

Answer. Ischemic heart disease occurs whenever there is an imbalance between myocardial oxygen demand and its supply.

Clinical Features Ischemic Heart Disease

1. Presence of asymptomatic ischemia.
2. Angina—Stable or unstable
3. Ischemic cardiomyopathy
4. Acute myocardial infarction
5. Cardiac arrest
6. Arrythmias or conduction defects
7. Sudden cardiac death
8. Asymptomatic coronary artery disease detected on routine medical check up.

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Risk Factors Ischemic Heart Disease

1. Age: As age advances chances of occurrence of coronary artery diseases increases. It is due to cumulative effcts of multiple risk factors overtime.
2. Diet: Diet rich in fat, sugar, cholesterol leads to formation of athroma and this leads to coronary artery diseases.
   Genetic: Positive family history of sudden death, myocardial infarction, angina are points to genetic predisposition.
3. Personality: In persons having traits of aggressiveness, ambition and competitiveness chances of occurrence of coronary artery diseases increases.
   Smoking: Persons who smoke are susceptible for coronary artery diseases because of nicotine and carbon monoxide.
4. Diabetes mellitus: Due to diabetes athroma may develop in early age and patient is suffring from asymptomatic coronary artery disease.
5. Obesity: It is associated with increased levels of serum cholesterol, blood pressure, serum triglycerides and serum insulin which lead to coronary artery disease.
6. Physical activity: Persons who does not undergo regular physical activities such as brisk walking or exercise have chances for coronary artery diseases.

Diagnosis Ischemic Heart Disease

In angina Pectoris

1. Resting ECG: ECG changes of myocardial ischemia are reflcted in S-T waves. Occasionally, there is flttning of T­waves in some lead in patient with angina.
2. Exercise ECG orStress test: Withcontinuous ECG monitoring and intermittntBP recordingis performed witha treadmill or bicycle ergometer.
   Standardised protocols are used (e.g. Bruce protocol), enabling performance to be assessed in same patient at diffrent times and work load at onset of symptoms or ECG changes to be determined. An exercise ECG is abnormal, if there is horizontal or down­sloping ST segment depression of 0.1 mm or more in any lead.
3. Myocardial perfusion scintigraphy: The isotope cardiovascular stress (usually thallium­201 or technetium—99 m) is injected at peak exercise and images taken with a camera immediately or shortly after exercise and compared with rest images taken a few hours later following a second injection of tracer.
   Areas of myocardial ischemia are identifid by reduced isotopic uptake in the same anatomical distribution stress images but not resting images (reversible defect).
4. Coronary angiography: It is done before angioplasty or coronary bypass surgery.

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In acute Myocardial Infarction  Ischemic Heart Disease

Diagnosis of acute myocardial infarction is based on history, characteristics symptoms and signs and investigations.

Investigations Ischemic Heart Disease

1. Electrocardiography:

1. ECG is the specific method for confirming the diagnosis.
2. Typical changes are seen in leads which faces the infracted area. These changes are:

1. Elevation of ST segment
2. Pathologic Q—waves appear.
3. T waves may become tall and peaked in very early myocardial infarction.
   T waves are transient and last for a few hours only.
4. In contrast to transmural lesions, partial thickness or subendothelial infarction causes ST/T wave changes without Q waves or prominent ST elevation.
5. Changes in the ECG are seen which evolve in predictable fashion over next few days to weeks.

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2. Blood test:

1. Plasma biochemical markers:

Myocardial infarction leads to detectable rise in the plasma concentration of various enzymes and proteins that are normally concentrated within the cardiac cells.
Plasma enzymes (cardiac injury enzymes) are as follows:

1. Creatine kinase (CK).
2. Aspartate aminotransferase (AST).
3. Lactate dehydrogenase (LDH).
4. Myoglobin
5. Troponins (troponin I and troponin T)

1. Creatine kinase starts to rise at 4–6 hours and it peaks by about 12 hours and falls to normal in 48–72 hours. Myocardial isoenzyme of creatine kinase is more specifi. It is useful for diagnosis of early myocardial infarction.
2. Aspartate aminotransferase (AST) starts to rise at about 12 hours and reaches a peak on the fist or second day and returns on third and fourth day.
3. Lactate dehydrogenase (LDH) starts to rise after 12 hours, reaches a peak after 2–3 days and may remain elevated for a week.
   Rise in the value of LDH I (an isoenzyme of LDH) is a more sensitive indicator of myocardial infarction than total LDH.
   It is useful in diagnosis for patients who present several days after myocardial infarction.
4. Cardiac troponins are cardiac troponin­T (cTn­T) and cardiac troponin­I (cTn­I). Sensitivity of troponins is similar to that of isoenzymes of creatine kinase. Moreover, cTn­T remains elevated for 100–200 hours after acute myocardial infarction and therefore, it may have particular utility in the evaluation of patients who present suffiently long episode after the pain in chest.

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2. Leucocytosis with a peak on fist day.

3. ESR is raised, which may remain raised for some days.

4. C-­reactive protein is elevated.

5. Chest X-ray: It can detect acute pulmonary edema or congestion. It is also helpful to detect pericardial effsion, cardiomegaly, etc.

6. Radionuclide scanning: It shows site of necrosis and the extent of impairment of ventricular function.

7. Echocardiography: This is done for regional wall motion abnormality and ejection fraction.

Management Ischemic Heart Disease

Angina pectoris is a symptom complex caused by transient myocardial ischemia and constitutes a clinical syndrome rather than a disease.

Types

1. Stable
2. Unstable
3. Nocturnal
4. Prinzmetal’s
5. Postinfarction angina

Etiology

Acute myocardial ischemia occurs when myocardial oxygen demand exceeds supply in following:

1. Coronary atherosclerotic narrowing (most cases).
2. Non­atherosclerotic coronary artery disease—Coronary spasm, coronary thromboembolism, congenital anomalies, coronary vasculitis.
3. Valvalar heart disease — Aortic stenosis and/or aortic regurgitation, mitral stenosis with pulmonary hypertension, mitral valve prolapse.
4. Pulmonary hypertension.
5. Systemic hypertension.
6. Hvpertrophic or dilated cardiomyopathy.
7. Anemia—from tachycardia and reduction in O2 availability.

Precipitating causes

1. Physical exertion
2. Heavy metal
3. Exposure to cold
4. Emotion and excitement
5. Hyperinsulinism in diabetic patients
6. Other causes: Straining at stools, bathing, sexual intercourse,micturition

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Clinical Features Ischemic Heart Disease

symptoms Ischemic Heart Disease

1. Anginal pain:

1. Site: Most often over middle or lower sternum or over left precordium, at times in epigastrium. Sometimes discomfort is located only in left shoulder or left upper arm, occasionally in lower jaw and rarely in interscapular area.
2. Radiation of pain: May spread to right or left arm or both neck or jaw. Occasionally, pain starts in the wrist, upper arms or face and then spreads to the chest.
3. Character: Vice­like constriction or choking. Sometimes only pressure or burning pain, rarely mere weakness of one or both arms. An important characteristic is its constancy, the pain being steady while it lasts.
4. Duration: Most commonly l to 4 minutes. It may force patient to stop walking.
5. Provocation: By effrt specially like walking against the wind or up a climb, hurrying after meals or unaccustomed exercise at times due to excitement anger, and fear. In advanced cases, pain is provoked by lying down (angina decubitus) or stooping.
6. Relief with sublingual nitroglycerine.

2. Dyspnea: If it occurs before the pain suggests severe ventricular disease.

3. Other symptoms:

1. Choking sensation in throat or feeling of impending doom.
2. Belching or passage of fltus or polyuria after an attck.
3. Dizziness, faintness or rarely syncope
4. If pain is severe sweating and nausea.

Signs Ischemic Heart Disease

1. At time, no signs are present.

2. Signs ofLV dysfunction: Atrial or third heart sound.

3. Dysfunction of papillary muscle: It can lead to transient mitral regurgitation in case of ischemia.

4. Signs associated with risk factors:

1. Hypertension.
2. Hyperlipidemia—Arcus senilis, xanthelasma, or cholesterol deposits along tendons and in skin of palms and buttcks.
3. Obesity
4. Diabetes and its accompaniments.

5. During the attck—pallor and sweating with rise of BP often tachycardia.
Pressure on carotid sinus may produce slowing of pulse and cessation of pain.

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Diagnosis Ischemic Heart Disease

Investigations Ischemic Heart Disease

1. Resting ECG: ECG changes of myocardial ischemia are reflcted in ST-T waves. Occassionally, there is flttning of T waves in some lead in patient with angina.
2. Exercise ECG or stress test: With continuous ECG monitoring and intermittent BP recording is performed with a treadmill or bicycle ergometer. Standardized protocols are used (e.g. Bruce protocol), enabling performance to be assessed in same patient at diffrent times and workload at onset of symptoms or ECG changes to be determined.
   An exercise ECG is abnormal, if there is horizontal or down­sloping ST segment depression of 0.1 mm or more in any lead.
3. Myocardial perfusion scintigraphy: The isotope cardiovascular stress (usually thallium­201 or technetium—99 m) is injected at peak exercise and images taken with a camera immediately or shortly after exercise and compared with rest images taken a few hours later following a second injection of tracer.
   Areas of myocardial ischemia are identifid by reduced isotopic uptake in the same anatomical distribution stress images but not resting images (reversible defect).
4. Coronary angiography: It is done before angioplasty or coronary bypass surgery.

Management Ischemic Heart Disease

1. It is divided into three phases:
2. General measures.
3. Pharmacological treatment.
4. Invasive treatment.

General Measures Ischemic Heart Disease

1. Do not smoke
2. Aim at ideal body weight
3. Take regular exercise
4. Avoid severe exertion, vigorous exercise and exercise in cold weather
5. Take sublingual nitrate before taking exertion that may induce angina.

Pharmacological treatment Ischemic Heart Disease

Following agents are used with successful outcome.

1. Antiplatelet agents:

1. Aspirin is used usually in dose of 75–150 mg daily.
2. Clopidogrel is used along with or without aspirin at dose of 75 mg daily.

2. Anti-anginal agents:

1. Sublingual glycertrinitrate effctively abort anginal attack by causing coronary vasodilatation and reducing preload and cardiac output.
2. Beta-blockers improve cardiac effiency and reduce oxygen consumption. Cardioselective agents such as atenolol 25 to 50 mg, metoprolol 200 mg daily can be used.
3. Calcium­channel antagonists, i.e. amlodipine, lacidipine. They are the vasodilators and lowers myocardial oxygen demand by reducing blood
   pressure and myocardial contractility.
4. Potassium­channel opener, i.e. nicorandil has atrial and venous dilatation property which does not exhibit tolerance.

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Invasive treatment Ischemic Heart Disease

1. *Percutaneous coronary *intervention or percutaneous transluminal coronary *angioplasty is done.
2. Coronary artery bypass grafting is done.

The management of myocardial infarction is divided into two parts:
1. Early management.
2. Late management.

Early Management Ischemic Heart Disease

1. Aspirin 150–300 mg to be chewed earliest.
2. Sublingual glyceryl trinitrate 0.4–1 mg, to be repeated, if necessary
3. Oxygen through nasal cannula at a rate of 2–4 L/min.
4. Procure IV line and take blood samples for glucose, lipids and complete haemogram.
5. Record 12­lead ECG.
6. Pain may be relieved by IV morphine (5 mg) plus metoclopramide as an antimetic (10 mg).
7. IV beta­blockers (metoprolol 5 mg every 2–5 minutes for 3 doses) for ongoing chest pain, hypertension and tachycardia provided there is no contraindication.
8. Thrombolysis should be done.
9. If PTCA is planned, give GP IIb/IIIa inhibitor
10. After admission immediately shift the patient to ICU or
    ICCU

In Hospital treatment Ischemic Heart Disease

Hospitalization and strict Bed rest

1. Hospitalize the patient and advice strict bed rest. As early as the patient is hospitalized, the bettr it is.
2. Patient should be strictly admittd in ICCU.

Analgesia Ischemic Heart Disease

1. IV morphine sulphate 10 mg and an anti emetic, i.e. cyclizine 50 mg is given through I.V. cannula.
2. The drug is repeated depending on the response till complete analgesia is received and patient feels bettr.

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Anti-platelet drugs Ischemic Heart Disease

Low dose aspirin, i.e. 75 to 150 mg and clopidogrel 300 mg stat and then 75 mg orally daily is given.

Oxygen therapy Ischemic Heart Disease

Inhalation of oxygen increases arterial partial pressure of oxygen, so there is increase in the concentration of oxygen gradient which is responsible for diffusionn of oxygen in ischemic myocardium from adjacent better perfused areas. This is given by facemask or nasal prongs for a day or two after infarction.

Thrombolysis Ischemic Heart Disease

1. Coronary thrombolysis helps to restore patency of coronary artery preserves left ventricular function and improves survival.
2. The choice of drug for thrombolysis is less important than the speed of treatment.
3. Streptokinase, 1.5 million units in 100 mL of saline given in an intravenous infusion over 1 hour, is a widely accepted method.
   It is a cheap, but being antigenic, sometimes, may cause serious allergic manifestations.
   Hence, it can be used once and therapy is changed if the patient requires second thrombolysis within few years.

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Alteplase (tissue Plasminagen activator (tPa)

1. It is a potent firinolytic drug but is expensive.
2. It is less antigenic and does not cause hypotension.
3. The current tPA regimen given over 90 minutes (bolus dose of 15 mg followed by 50 mg over 30 minutes and then 35 mg over next 60 minutes) is widely accepted. The other drugs include reteplase given in double dose regime i.e.
   10 million units over 2–3 minute followed by another dose of 10 million units after 30 minutes.
   Tenectaplase given as bolus dose of 53 mg/kg over 10 seconds. Both reteplase and tenectaplase are known as bolus firinolytics.

Angioplasty Ischemic Heart Disease
Immediate angioplasty of infarct related artery is safe and is effctive alternative to thrombolysis. It is done in the patients in whom the hazards of thrombolysis is high.

Anti-coagulants Ischemic Heart Disease

1. Sub­cutaneous heparin, i.e. 7,500 units twice a day for 7–10 days or till discharge of patient from the hospital can be employed.
   In patients who do not receive thrombolytic therapy to prevent venous thrombosis.
2. Patients who receive thrombolytic therapy (tPA) should receive immediate and full doses of heparin (10,000 U bolus plus, l000 U hourly).

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Beta-adrenergic Blockers Ischemic Heart Disease

Acute beta­adrenoreceptors blockade intravenous atenolol (5–l0 mg given over 5 minutes) or metoprolol (5–15 mg given over 5 minutes) relieves pain, reduces arrhythmias, salvages myocardium and improves short term mortality in patients who present within l2 hours of onset of pain.

Nitrates and other agents Ischemic Heart Disease

Sublingual glyceryl trinitrate 0.4 mg is useful in threatened infarction.

Sedatives Ischemic Heart Disease

Diazepam 5mg for three to four times a day is effctive. It is given for few days.

Diet Ischemic Heart Disease

1. For fist 4 to 5 days low calorie diet which is divided into multiple meals is given.
2. If heart failure is present restrict the salt.
3. From second week, food should be increased in amount.

Lipid lowering agent Ischemic Heart Disease
Atorvastatin is given to reduce the LDL levels.

Late Management Ischemic Heart Disease

1. Risk stratifiation and further investigations: Prognosis of patient survived after myocardial infarction depends on degree of myocardial damage, any residual ischemia and presence of ventricular arrhythmias.

2. Life style modifiation:

1. Stop smoking
2. Diet control
3. Regular exercise.

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3. Secondary prevention

1. Antiplatelet agents, i.e. aspirin
2. Lipid lowering agents
3. Beta­blockers and ACEI in congestive cardiac failure and hypertension.
4. Control of blood sugar in diabetes.

4. Rehabilitation and after care:

1. Physical activities should be restricted for 4 to 6 weeks since infarct takes 4–6 weeks to become replaced with firous tissue.
2. Gradual mobilization and return to work over 6 weeks.
   When there are complications, the regimen has to be modifid accordingly.
3. Exercise within the limits set by angina and tiredness will do no harm but much good. Same limits apply to sexual activity.
4. Control of obesity, regular exercises, cessation of smoking, adoption of a less frenetic way of life and control of plasma lipids by diets and drugs.
5. Complications should be managed. Pain relief, reassurance, rest and correction of hypokalemia play a major role in prevention of arrhythmias.

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Routine drug therapy Ischemic Heart Disease

1. Low dose aspirin, i.e. 75 to 150 mg daily and is continued indefiitely.
2. Beta-adrenergic blocker should be given for 4 to 6 weeks if there is no contraindication.
3. ACE inhibitor, i.e. captopril 25 mg TID or ramipril 2.5 to 5 mg BD
4. Lipid lowering agent atorvastatin is given to lower the LDL levels.