Ischemic heart disease is defined as inadequate blood supply and oxygen to the myocardium. Typically happens when demand and supply mismatch.
A global trend of ischemic heart disease
Ischemic heart disease causes high mortality and financial burden on the community. In the united state, 15.5 million people have Ischemic heart disease, and 3.4 persons have angina pectoris. Many factors contribute to Ischemic heart disease such as gene, obesity, high-calorie diet, smoking, and sedentary life-style. In 2020, Ischemic heart disease would be the most common cause of death worldwide.
Coronary atherosclerosis in ischemic heart disease
The major atherosclerotic site is the epicardial coronary artery. High LDL (low-density lipoprotein), low HDL (high-density lipoprotein), cigarette smoking, blood pressure, diabetes mellitus are the risk factors. It can change the vascular tone, inflammation of the endothelium. Vulnerable vessels and vulnerable blood combination promote a state hypercoagulability and hypofibrinolysis as in diabetes.
When the coronary artery ruptures and separating plaque which activates the platelet and coagulation cascade. Leading to fibrin deposition and causes myocardial ischemia. The left main and left proximal anterior coronary artery is a more critical obstruction. Progressive stenosis leads to a pressure gradient across the proximal, and post stenosis pressure fall.
Effects of ischemia in ischemic heart disease
Inadequate perfusion may cause transient disturbance of the mechanical, biochemical, and electrical function of the myocardium. Coronary atherosclerosis causes nonuniform ischemia resulted in to decrease ventricular contraction. The myocardium metabolized fatty acids and glucose to carbon dioxide and water. Due to severe hypoxia, free fatty acids cannot be oxidized, and glucose is converted to lactate.
As a result of this, Ph is decreased, potassium leak, and sodium and calcium uptake are increased by myocytes. ECG changes evidenced by T inversion reflect non-transmural, intramyocardial ischemia; ST segment depression reflects subendocardium ischemia; ST-segment elevation caused by severe transmural ischemia.
|class||New York heart association functional classification|
|1||The patient has the cardiac disease but without limitation of physical activity. Ordinary physical activity does not cause fatigue, palpitation, dyspnea, or angina pain.|
|2||Patients have cardiac disease resulting in slight limitation.|
|3||Cardiac disease with marked limitation|
|4||Cardiac disease with the inability to carry any physical activity.|
The man >50 and women >60 who complains heaviness, squeezing, smothering. Although an episode of angina caused by exertion and relieved by rest. The threshold for angina may vary from time of day and emotional state. Exertional angina is relived in 1-5 min by slowing or stopping activities and even by rest and sublingual nitroglycerine. The history of typical angina pectoris establishes the diagnosis of IHD until proven otherwise.
Stress testing for ischemic heart disease
The diagnosis of Ischemic heart disease and estimation of risk and prognosis will do the 12 lead ECG before, during, and after exercise, usually on a treadmill. The test consists of incremental external workload while symptoms, the ECG, blood pressure is monitored. The test is discontinued when chest discomfort, breathlessness, fatigue, ST-segment >2 depression, systolic blood pressure >10 mmHg, ventricular tachycardia.
A positive result on exercise probably 98% have coronary artery disease. Contraindication of tests is resting angina within 48 hours, unstable rhythm, severe aortic stenosis, acute myocarditis, uncontrolled heart failure, severe pulmonary hypertension, and active infective endocarditis.
Cardiac imagine in ischemic heart disease
Abnormal ECG changes following the treadmill test to gain more information about cardiac function cardiac imagine are useful. Myocardial radionuclide perfusion imagines after thallium 201 or 99m-technetium sestamibi during the exercise test.
Coronary arteriography for ischemic heart disease
This is a diagnostic method for coronary integrity. However, coronary arteriography provides no information about arterial walls, severe atherosclerosis.
- Chronic stable angina with severely symptomatic despite medical therapy
- Troublesome symptoms that can rule out IHD
- Angina patient survived on cardiac arrest
- Cardiac dysfunction
- High risk of a coronary event
Prognosis of ischemic heart disease
Prognostic indicators in Ischemic heart disease are age, functional state of the left ventricle, location, and severity of coronary narrowing, myocardial ischemia. Recent onset angina, MI, unresponsive to medical therapy, uncontrolled heart failure are increase risk of acute coronary events.
treatment of sable angina pectoris
Evaluate the patient according to his /her understanding, expectation, goals, and prevention of adverse outcomes.
- Explain the problem and reassurance with the formulation of the treatment plan
- Identify aggravating factors and treat them
- Treatment of risk factors
- Medical therapy for angina
- Consider for revascularization.
- Recommend activity which reduces symptoms
Explanation and reassurance in ischemic heart disease
The patient should understand their condition and realized that productive life can be possible with angina disease. Planed rehabilitation can encourage patients to lose weight, improve exercise tolerance, and control risk factors.
Identification and treatment of the aggravating condition
A condition that increases or decreases oxygen demand that precipitates angina in IHD. Hypertrophic cardiomyopathy, aortic valve disease, LVH may cause angina and should be treated. Obesity, hypertension, hyperthyroidism should be treated effectively.
Adaptation of activity in ischemic heart disease
Myocardial ischemia is caused by an imbalance between the demand and supply of oxygen. Angina patients need to accomplished without symptoms by reducing the speed of work. Metabolic equivalent tasks (METs) are the numbers that patients can perform daily activities that will fall below the ischemic threshold.
|Less than 3 MET||3-5 METs||5-7 METs||7-9 METs||>9 METs|
|Washing, dressing, light housekeeping, desk work, driving auto||Cleaning windows, raking, power lawn mowing, bed making, carrying object (15-30) lb||Easy digging, lavel hand lawn moving, carrying object 30-60 lb||Heavy shoveling, Carrying object 60-90 lb||Carrying load up stair >90 lb|
|Sitting, standing, desk work,||Stocking shelves, welding||Carpentry, sawing wood||Digging ditches||Heavy labour|
|Golf, knitting||Dancing, golf, sailing, tennis||Tennis, snow skiing basketball,||Mountain climbing||squash|
|Walking 2 mph, biking,||Level walking 4 mph, biking 6-8 mph||Level walking 5 mph, bicycling 9-10 mph, swimming||Level jogging, swimming, rowing machine,||Running> 6mph, bicycling > 13 mph, rope jumping.|
Treatment of risk factors of ischemic heart disease
A family history of Ischemic heart disease has increased risk and should treat risk factors such as hyperlipidemia, hypertension, and diabetes. Cigarette smoking provokes the risk of thrombosis, plaque instability, myocardial infarction, and death.
Hypertension has increased the risk of coronary atherosclerosis as well as stroke. Diabetes mellitus accelerates coronary and peripheral atherosclerosis and associated with dyslipidemia.
The main aim to treat dyslipidemia is long-term relief from angina, decrease the need for revascularization, reduction in myocardial infarction, and death. Control of dyslipidemia is achieved by low saturated and trans saturated fatty acid, exercise, and weight loss. Statins, fibrate, or niacin is used to treat dyslipidemia. Injectable monoclonal antibodies against PCSK9 available to dramatically lowering LDL cholesterol.
Risk reduction in women with Ischemic heart disease
The atherosclerotic changes increase after menopause. Risk factors that accumulate condition are cigarette smoking, diabetes, hypertension, dyslipidemia.
Drug therapy of ischemic heart disease
Commonly used drugs for treatment of IHD .
|Nitrate therapy in patient with ischemic heart disease|
|Nitroglycerine Ointment |
Transdermal patch Sublingual Tablet
| 0.5-2 in |
0.2-0.8 mg/h 0.3-0.6 mg
1 or 2 spary
|Two or three times Od Sos sos|
|Isosorbide dinitrate Oral |
Oral sustained releasse
| 10-40 mg |
|Bd or tid Od or bd|
|Isosorbide 5- mononitrate Oral Oral sustained release|| 20 mg |
The mechanism of action of nitrate is venodilation with a reduction in LV end-diastolic volume and pressure. Therefore, reducing muscle wall tension and o2 consumption. Nitrate also has an antithrombotic property by an inactivating platelet. Absorption occurs through mucous membranes and is rapid. So can be used sublingually an angina episode.
|Betablocker used in ischemic heart disease|
|Labetolol||200-600 mg bd|
|Propranolol||80-120 mg bd|
These drugs reduce myocardial oxygen demand by inhibiting increased heart rate, arterial pressure, and myocardial contractility. The therapeutic aim is to reduce angina attacks.
In addition, it can reduce the mortality and re-infraction rate in post-myocardial patients and moderately antihypertensive effects. A relative contraindication is asthma reversible chronic lung disease AV conduction defect, severe bradycardia, Raynaud’s phenomenon, and mental depression.
|Calcium channel blocker used in Ischemic heart disease|
| 5-10 mg od |
| 120-320 mg|
CCB is a coronary vasodilator and as effective as beta-blockers in the treatment of angina. They are indicated when beta-blocker is contraindicated, poorly tolerated, or ineffective. Verapamil and diltiazem might produce an asymptomatic disturbance in conduction.
Also, aggravate LV dysfunction. Although, useful effects are achieved by a combination of beta-blocker and CCB. Verapamil should not be combined with beta-blocker due to the aggravation of side effects.
Beta-blocker has shown to improve life expectancy after acute myocardial infarction. However CCB is indicated in inadequate response to beta-blocker and nitrate, adverse reaction to beta-blocker, angina with a history of asthma, sick sinus syndrome, Prinzmetal’s angina, PVD.
Antiplatelet drugs in ischemic heart disease
Aspirin is an irreversible cyclooxygenase inhibitor so interfere with platelet activation. Chronic consumption of 75-325 mg orally has been shown to reduce coronary events. A dose-dependent increase in bleeding when used chronically so preferably used an enteric-coated tablet in the range of 81-162 mg/day.
Clopidogrel has blocked P2Y12 ADP receptor-mediated platelet aggregation with loading 300-600 mg and 75 mg/day. Alternative agents that block P2Y12 are prasugrel and ticagrelor and shown more effective than clopidogrel. Although, aspirin and clopidogrel combination is recommended in patients with acute myocardial infarction.
Other therapy in ischemic heart disease
ACE inhibitors used in patients with increased risk especially diabetes mellitus, left ventricular failure, high blood pressure, high LDL cholesterol on beta-blocker, and statin.
Ranolazine and piperazine may be useful for chronic angina despite standard medical therapy. It inhibits sodium channel and limits Na overload and prevention of calcium overload.
NSAID may be used in IHD but co administered with aspirin.
Another agent is ATP sensitive potassium channel opener Nicorandil, 20 mg BID for the prevention of angina.
Ivabradine 2.5-7.5 mg BID is specific sinus node inhibiting agent may be beneficial to reduce cardiovascular event.
Angina and heart failure
Left ventricular failure with angina can be controlled by nitrates. Congestive heart failure with ACE, diuretic, and digoxin reduces heart size, wall tension, and myocardial oxygen demand. Trial of short-acting esmolol may be useful to establish the safety of bet blockers in the selected patients.
Cardiac catheterization and coronary revascularization need to be done if CCF and angina in combination.
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Dr Manish Khokhar