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• Myocardial ischemia most often develops as a result of reduced blood supply, due to atherosclerotic plaques, to a portion of the myocardium.
• Angina that is reproduced by exercise, eating, and/or stress and is subsequently relieved with rest and without recent change in frequency or severity of activity necessary to produce symptoms is called chronic stable angina.
• Clinical characteristics associated with a poor prognosis include older age, male sex, prior MI, diabetes, hypertension, and multiple-vessel or left-mainstem disease.
• Males predominate in those younger than 70 years. This is due to the cardioprotective effect of estrogen in females. At 15 years postmenopause, incidence of angina occurs with equal frequency in both sexes.
• Between ages 40-70 years, angina is diagnosed more often in males than females. After age 70 years, females are affected equally.

• Atherosclerotic plaque disease is the predominant cause. Coronary artery vasospasm is less common.
• Alternative causes of angina include the following:
• Ventricular hypertrophy due to hypertension, valvular disease, or cardiomyopathy
• Embolic occlusion of the coronary arteries
• Hypoxia, as in carbon monoxide poisoning or acute pulmonary disorders
• Cocaine and amphetamines, which increase myocardial oxygen demand and may cause coronary vasospasm
• Underlying coronary artery disease, which may be unmasked by severe anemia

• Not all patients experience chest pain. Other symptoms, such as shortness of breath or severe weakness, may represent anginal equivalent symptoms.
• Patients may complain of the following:
• Palpitations
• Pain, which is usually described as pressure, squeezing, or a burning sensation across the precordium, may radiate to neck, shoulder, jaw, back, upper abdomen, or either arm.
• Exertional dyspnea that resolves with pain or rest
• Nausea from vagal stimulation
• Diaphoresis from sympathetic discharge
• Decreased exercise tolerance
• Diabetic and elderly patients are more likely to have atypical presentations and offer only vague complaints, such as weakness, lightheadedness, and nausea.

• Involves episodic pain lasting 5-15 minutes
• Provoked by exertion
• Relieved by rest or nitroglycerin

• Patients have increased risk for adverse cardiac events, such as MI or death.
• New onset exertional angina
• Angina of increasing frequency or duration or refractory to nitroglycerin
• Angina at rest

• Occurs primarily at rest
• Triggered by smoking
• Thought to be due to coronary vasospasm

• The physical exam is frequently normal. If chest pain is ongoing, the patient usually will lie quietly in bed and may appear anxious, diaphoretic, and pale.
• Hypertension may precipitate angina or reflect elevated catecholamines due to either anxiety or exogenous sympathomimetics.
• Hypotension indicates ventricular dysfunction due to ischemia or acute valvular dysfunction.
• Indicators of Congestive heart failure (CHF)
• Jugular venous distention
• Third heart sound (S3)
• New murmur, papillary muscle dysfunction
• Rales on pulmonary exam suggest LV dysfunction or mitral regurgitation.
• Presence of a fourth heart sound (S4) is a common finding in patients with poor ventricular compliance due to preexisting ischemic heart disease or hypertension.

 

• ECG is the most important diagnostic test for angina.
• A normal ECG or one that remains unchanged from the baseline does not exclude the possibility that chest pain is ischemic in origin.
• Changes that may be seen during anginal episodes include the following:
• Transient systolic time (ST) elevations (fixed changes suggest acute MI)
• Dynamic T-wave changes, either inversions, normalizations, or hyperacute changes
• ST depressions that may be junctional, downsloping, or horizontal
• Diagnostic sensitivity may be increased by performing right-sided leads (V4R), posterior leads (V8, V9), and serial recordings.
• Creatine kinase fraction (CK-MB) is the gold standard for detection of myocardial necrosis.
• Levels in acute MI begin to rise within 4 hours of injury, peak at 18-24 hours, and subside over 3-4 days.
• The upper limit of normal for CK-MB is 3-6% of total CK. A normal level in the ED does not exclude the possibility of myocardial necrosis.
• A single assay has a 34% sensitivity for acute MI. Serial sampling over periods of 6-9 hours will increase sensitivity to approximately 90%. Serial CK-MB over 24 hours will detect myocardial necrosis with a sensitivity near 100% and a specificity of 98%.
• Check CK-MB on those patients with prolonged episodes of ischemic pain, patients with new changes on ECG, or patients with nondiagnostic ECGs.
• Troponin I is a contractile protein normally not found in serum. Within the first 6 hours, its sensitivity is superior to CK-MB for detection of myocardial necrosis.
• Troponin I is detectable in serum 3-6 hours after necrosis and remains elevated for 14 days.
• In patients with unstable angina, minor elevations may identify patients at risk for subsequent cardiac events (eg, acute MI) and death.
• Troponin T releases kinetics similar to troponin I, but it is less sensitive than troponin I for detection of early myocardial necrosis.
• Echocardiogram

• An echocardiogram often demonstrates wall motion abnormalities due to ischemia.

• The goals of treatment are to preserve patency of the coronary artery, augment blood flow through stenotic lesions, and reduce myocardial oxygen demand.
• All patients should receive antiplatelet agents, and patients with evidence of ongoing ischemia should receive aggressive medical intervention until signs of ischemia, as determined by symptoms and ECG, resolve.
• Patients with severe unstable angina and ECG changes should be admitted to a telemetry
• Patients with symptoms refractory to aggressive medical treatment, shock, suspected or known aortic stenosis, or new or worsening mitral regurgitation are at high risk.
• Patients with chronic stable angina may be considered for discharge after occurrence of the following:
• Symptom duration is brief and identical to symptoms experienced in the past.
• ECG is normal or unchanged.
• Patient has access to timely follow-up with a primary care MD.
• Use ticlopidine 250 mg PO bid as a substitute for patients unable to take aspirin because of a history of hypersensitivity or bleeding.
• Metoprolol and propranolol are excellent choices for inpatient and outpatient management.
• Use esmolol for inpatient treatment, particularly those at risk for adverse side effects from beta-blockade.

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• Prognosis is generally excellent. Factors that have been shown to improve prognosis include the following:
• Aspirin reduces progression to both nonfatal MI and cardiac death.
• Beta-blockers control anginal symptoms and reduce cardiac complications in patients with hypertension.
• PTCA and revascularization improve the prognosis in high-risk patients.
• Poor prognostic factors include male sex, diabetes, and hypertension.
• Factors associated with a poorer prognosis include the following:
• Evidence of myocardial necrosis, as determined by elevated troponin T
• Delays in angiography in high-risk patients (Early angiography allows for triage to medical therapy, PTCA, or revascularization.)
• Patients with cocaine-related ischemia

Results from prolonged myocardial ischaemia precipated by –

• Mostly – Occlusive coronary thumbus at the site of preexisting atherosclerotic plaque

• Prolonged vasospasm

Location of infarction:

• Thrombosis in Ant. Descending branch of Left coronary artery – Ant left ventricle & intervertricular septum
• Left circumflex artery – Antero or posterolateral infarction
• Right coronary thrombosis – Posteroinferior portion of left ventricle and Right ventricle and interventricular septum

• Precordial pain – 30% patients give history of alteration in pattern of angina or unusual indigestion felt in chest
• Pain of infarction –Mostly at rest – sensation of tightness, squeezing, burning choking, acting pain or ill – characterised by discomfort felt behind left shoulder & upper arm
• Anxiety , vomiting, Breathlessness, syncope
• Painless infarction – Can occur In about 25% of patients
• Sudden death – In about 20% patients in the first attack

• Of sympathetic activation – pallor, sweating , tachycardia
• Of vagal activation – Bradycardia, vomiting
• Respiratory distress, fever
• Rates or diffuse wheezing suggests pulmonary edema
• Heart – Raised JVP, Atrial gallops (S4) common and ventricular gallops(S3) less common

• Mitral regurgitation murmurs – indicate papillary muscle dysfunction

• Classic evolution of changes are peaked T waves to ST segment elevation to Q wave development to T wave inversion.
• Q waves do not occur in 30-50% of infraction. These patients with T wave & ST changes with elevated plasma enzyme are called non Q wave infarctions

• Creatine kinase (CK) Aspartate aminotranferase (AST) Lactate dehydrogenase (LDH).

• AST rises by 12 hrs, peak –I or II day, Normal by 3-4 days.
• LDH rises by 12 hrs, peak – 2-3 days, elevated for a week

• Shows complications like aneurysms, septal dyskinesia, luminal thrombosis.

Scintigraphy studies –

• Technetium – 99 pyrophosphate scintigraphy to diagnose Acute M.I
• Shows ‘hot spot’ image of infarction but not effective in detection of small infarction.
• Radiolabelled antimyosin antibody are more sensitive and specific
• Scintigraphy with thallium – 201 – demonstrates cold spots in regions of diminished perfusion.

• Bed rest
• High flow O2
• Thrombolytic therapy :

1. Greatest benefit if initiated within first 3 hours

Streptokinase -- #9; 20min 1.5 million IV drug

Tissue Plasminogen -- #9; 5min 100 mg Bolus

Activator (t PA)

Reteplex 15min #9; #9; #9; 20 units bolus

Setreptokinase produces allergic reations like anaphylaxis, fever, rashes

When used along with tPA– cerebral hemorrhage is more common.

1. Acute PTCA – if no response to medical treatment, for single vessel disease and non calcified atheroma.
2. Analgesia – Sublingual nitroglycerin initially morphine sulfate 4-8 mg or meperidine 50-75 mg
3. B-adrenergic blocking drugs – IV atenolol 5-10 mg or IV metoprolol – 5-15 mg

 

4. ACE inhibitors - patients with low ejection fractions, large infarctions and with heart failure benefited maximally.
5. Antiarrythmic prophylaxis – with liodocaine infusion

 

6. Calcium channel blockers – In patients with non Q wave infarction.

• Infarct extension and post infarction ischemia – twice common in non Q wave infarction
• Arrythmia
• Sinus bradycardia – Most common in inferior infarction If low cardiac output – give 0.5 -1mg atropine I.V
• Supraventricular tachyarrythmias - sinus tachycardia is common
• Beta blocker – propranolol (1-2mg) metoprolol (2.5-5mg)
• Verapamil (2.5-5mg) or diltiazem(5-15 mg) given if Beta – blockers are contraindicated
• Digoxin to be started if heart failure is present with atrial fibrillation electrial cardioversion
• Ventricular arrhythmias-

• Conduction disturbances-

• Myocardial dysfunction

Acute left ventricular failure: digoxin are usually effective

furosemide (10-40mg) or Bumetamide (0.5 –1 mg) is given

• Myocardial rupture
• Left ventricular aneurysm
• Pericarditis
• Mural thrombosis.