CAD

Coronary Artery Disease

Atherosclerosis is the leading cause of death and disability in the developed and developing world Clinical manifestations depend on the particular vascular bed affected Coronary vasculature angina, MI, sudden death Cerebral TIA, stroke Peripheral claudication, gangrene Renal hypertension


Disease impact: In 1997, more than 5mn Americans had CVD Currently one in five American has some form of CVD Each year 1mn deaths are due to CVD (42% of all deaths!) One-sixth of CVD deaths are in persons <65 yrs of age Annually 1.5mn Americans have MI 0.5mn die from CHD 0.5mn have stroke 0.15mn die from stroke

Death rates from CHD has decreased by 40% since 1968 CVD still remains the leading cause of death in developed nations CHD & stroke are the 2nd and 3rd leading causes of mortality even in the developing regions

Pathophysiology

CAD is almost always due Atherosclerosis. Occasionally, other such as aortitis, polyarteritisAtherosclerosis is a progressive inflammatory disorder of the arterial wall that is characterised by focal lipidrich deposits of atheroma.Development of lesions, starting in childhood, progress through phases, caused by injury to intima of arteryPhase I : fatty streaks – do not obstruct flowPhase II: fibrous plaque- elevated lesion protruding into lumen obstructs flow to varying degreesPhase III: complicated lesions – partially or totally occlude lumen


Non-modifiable risk factorsAge: death from CAD  with ageSexFamily historyRace: afro-Americans have = 45% > hypertension than Caucasians Risk factors

Coronary Artery Disease

Modifiable Risk FactorsCigarette smoking: 2X increased risk for CADHTN: damages blood vessels leading to plaque formation and atherosclerosisHyperlipidemia: CAD and atherosclerosis by causing build up in artery wallsPhysical Inactivity: risk of CAD 2XDiabetes:  risk 2X in men; 3X in womenObesityStress : increased catecholamine release;  sympathetic response


Spectrum of coronary artery disease -Silent ischemia -Chronic stable angina -Acute coronary syndromes Unstable angina NSTEMI STEMI -Heart failure -Arrhythmia -Sudden death

Chronic stable angina

Angina pectoris is the clinical syndrome caused by transient myocardial ischaemia. It may occur whenever there is an imbalance between myocardial oxygen supply and demand. Coronary atheroma is by far the most common cause of angina.

Chronic stable angina

Chest discomfort caused by transient myocardial ischemia without cell deathUsually brought on by  physical or emotional stress and promptly relieved by rest.Precipitated by 4 “E’s”Extreme emotionExtreme temperatureExcessive eatingExerciseCoronary atheroma is by far the most common cause of angina.Physical examination is frequently unremarkable.

Investigations

Resting ECG often normal. Exercise ECG. Myocardial perfusion scanning. Stress echocardiography. Coronary arteriography

Management

Risk factors modification such as smoking, hypertension and hyperlipidaemia. Drugs Antiplatelet therapy Low-dose aspirin reduces the risk of adverse events such as MI and should be prescribed for all patients with coronary artery disease indefinitely .Clopidogrel (75 mg daily) is an equally effective. Anti-anginal drug treatment Nitrates Beta-blockers

Calcium channel antagonists Potassium channel activators Invasive treatment Percutaneous coronary intervention PCI. CABG

Acute coronary syndrome

Acute coronary syndrome is a term that encompasses both unstable angina and myocardial infarction (MI). It is characterised by new-onset or rapidly worsening angina (crescendo angina), angina on minimal exertion or angina at rest in the absence of myocardial damage. In contrast, MI occurs when symptoms occur at rest and there is evidence of myocardial necrosis, as demonstrated by an elevation in cardiac troponin or creatinekinase-MB isoenzym.



Acute myocardial infarction (AMI) One of the most common diagnosis in hospitalized patients in industrialized nations Mortality of acute MI is 30% and one-half of these deaths occur before hospitalization Mortality after admission has decreased by 30% in last 2 decades


Pathophysiology AMI results when thrombus (occlusive/nonocclusive) develops at the site of ruptured plaque
Vulnerable plaque Rupture
Coagulation cascade platelet adhesion, activation activation,aggregation
Fibrin and platelet clot Coronary occlusion MI


Presentation:Chest pain- most common, similar to anginal pain but more severe and prolonged described as severe, crushing/squeezing/pressure ‘worst pain’ everChest pain may be absent in pts with DM or in elderlyAtypical presentations:confusion, syncope, profound weakness, arrhythmia

Differential diagnosis: Pericarditis Pulmonary embolism Pneumothorax Aortic dissection Esophageal spasm

Examination: Anxiety, pallor, restlessness Substernal chest pain with diaphoresis is strongly suggestive of AMI Those with anterior MI may have sympathetic overactivity whereas those with inferior MI may have para- sympathetic overactivity S3/S4 Transient systolic murmur due to dysfunction of mitral apparatus leading to mitral regurgitation

Laboratory findings: ECG specific but insensitive tool for diagnosis of myocardial ischemia Total occlusion of infarct related artery leads to ST elevation (STEMI) and subsequent evolution of Q waves Partial occlusion/early recanalization/rich collaterals leads to NSTEMI (non-ST elevation MI)

Serum cardiac markers: Released into the circulation from necrotic heart muscle: CK (creatine kinase) rises 4-8 hrs after onset of MI And normalize by 48-72 hrs not specific for myocardial necrosis MB isoenzyme of CK is more specific Cardiac specific troponins: more sensitive and specific than CK and CKMB for identification of myocardial necrosis Myoglobin- first serum marker to rise after MI, but lacks specificity.



Cardiac Enzymes


Cardiac imaging 2D echocardiography reveals regional wall motion abnormality also useful to identify mechanical complications of MI Radionuclide imaging used infrequently in the diagnosis of acute MI mainly used to risk stratify patients with CHD

Management Prehospital care: Major elements include Recognition of symptoms by the patient and prompt medical attention Rapid deployment of EMS capable of resuscitation and defibrillation

Goals of Initial management in ED Control of cardiac pain Rapid identification of patients suitable for reperfusion Triage of low risk patients for subsequent care Avoiding inappropriate discharge of patients with MI


Initial management Focused history and Focused examination Reassurance Ensure IV access + Basic investigations Aspirin: 160-325 mg chewable aspirin + Clopidogril Oxygen by nasal cannula if hypoxemia is present Sublingual nitroglycerine followed by IV infusion if needed Intravenous beta blockers (decrease myocardial oxygen demand, control chest pain and reduce mortality) Morphine for pain relief (given IV in small doses)+ Metelopromide Monitor 12 Leads ECG Consider Reperfusion

Reperfusion therapy

Primary percutaneous coronary intervention (PCI). Thrombolysis.

Absolute Contraindications• Any prior intracranial hemorrhage• Known structural cerebral vascular lesion (e.g., AV malformation)• Malignant intracranial neoplasm• Ischemic stroke in last 3 months• Suspected aortic dissection• Active bleeding or bleeding diathesis• Closed head or facial trauma in last 3 months

Relative Contraindications• Recent (3 weeks) major surgery• Recent (3 weeks) trauma• Cardiopulmonary resuscitation of >10min• BP > 180/110• Ischemic stroke more than 3 months old• Internal bleeding in last month• Noncompressible vascular punctures• For streptokinase/Anistreplase: prior exposure or allergy• Pregnancy• Active peptic ulcer• Currently on anticoagulants (sodium warfarin, Coumadin); the higher the INR, the higher the risk

STEMI

ASA, beta blockers, antithrombin therapy
<12 hrs >12 hrs
Eligible for Lytic therapy
Lytic C/I
Not a candidate For reperfusion
Persistent symptoms
Thrombolysis Primary PCI no yes
Other medical therapy Consider reperfusion (ACEI, nitrates, beta blockers, antiplatelets, antithrombin,statins)


Time is muscle

Complications of acutecoronary syndrome

Arrhythmias VF,AF, BRADYCARDIA Ischemia Acute circulatory failure Pericarditis Mechanical complications Embolism Impaired ventricular function HF Ventricular aneurysm


Unstable angina/NSTEMI Aspirin, anticoagulants, nitrates, GP IIb-IIIa antagonist Betablockers(calcium channel blockers) Assess clinical status
High risk/unstable Stable
(Recurrent ischemia, LV dysfunction Widespread EKG changes, positive enzyme markers)
Cardiac catheterization Severe ischemia
Revascularization (PCI/CABG) Medical therapy
Stress test
yes
no

Maintanance Therapy

Life style changes Aspirin Clopidogril B blocker ACE inhibitors Calcium channel blocker Statins ( Antilipids)