Coupon Accepted Successfully!


Coronary Artery Disease (Ref. Hari. 18th ed., pg - 1998)

Angina Pectoris


Basic physiology

  1. Coronary flow is maximum at early diastole.
  2. 80% of the coronary filling occurs during diastole.
  3. In aorta, blood flow drops maximum at the end of diastole. 

Angina Pectoris is best diagnosed by history. (AIPG 2010)

  1. This is due to myocardial ischaemia and presents as a central chest tightness or heaviness (Levine sign) which is brought on by exertion and relieved by rest.
  2. It may radiate to one or both arms ,the neck, jaw or teeth. Atherosclerosis is the most common cause of CAD.
  3. ECG and Echo may be normal and cardiac enzyme are usually not raised in angina. 

Unstable angina (Ref. Hari. 18th ed., Pg-2015)



  1. Pts with new onset angina ( 4 - 6 weeks) that is severe and/or frequency (>3 episodes/day) Q
  2. Pts with accelerating angina–prolonged, more frequent, severe or precipitated by less exertion than previously Q
  3. Pts with angina at rest Q or by minimal exertion usually lasting for >10 mints. 

Important Points:

  1. Variant (Prinzmetal's) angina: caused by coronary artery spasm Q. Patient has pain chest at rest & ECG show ST segment elevation. Treatment Ca channel blocker and nitrates but beta blockers are Contraindicated.
  2. Microvascular angina: In this case patient has symptoms of angina i.e. he has pain chest which is precipitated by exertion. But he has normal coronary angiography. It occurs due to abnormal constriction or failure of relaxation of coronary resistance vessels. (Slow flow phenomena) 

Important Points:



  1. ECG: usually normal but may show ST depression; flat or inverted T waves'.
  2. If resting ECG is normal, then do exercise ECG 

Criteria of positive TMT

  1. Appearance of horizontal or ST depression > 1 mm lasting for > 0.08 Sec
  2. Systolic fall of BP > 10mmHg
  3. Development of VT 

Extra Edge: An abnormal ST segment on a resting ECG, as seen in LBBB, LVH, or the use of digoxin by the patient all reduce the accuracy of this test.


Extra Edge: Those patients who can not run on the TMT machine than drug induce stress test is done by using injection dobutamine


Angiography – If TMT is positive than the next investigation is angiography.


TIMI Risk Score for Unstable Angina (UA) /Non ST elevated MI (NSTEMI)


It estimates mortality for patients with unstable angina and non-ST elevation MI.


The factors are:

  1. Age ≥ 65 years                               
  2. ≥ 3 Risk Factors for CAD             
  3. Known CAD (stenosis ≥ 50%)                  
  4. Aspirin Use in Past 7d   
  5. Severe angina (≥ 2 episodes w/in 24 hrs)         
  6. ST changes ≥ 0.5mm   
  7. Elevated Cardiac Marker      

Recent Advances: Pathology of Plaque. 

  1. Atherosclerotic plaques become progressively calcified over time, increases with age.
  2. For this reason, methods for detecting coronary calcium have been developed as a measure of the presence of  coronary atherosclerosis.
  3. Detection of calcium in atherosclerotic plaque by electron beam CT scan (EBCT).  
  4. Coronary calcium detected by these imaging techniques is quantified using the Agatston score most  commonly, which is based on the area and density of calcification.

Recent Advances:

  1. LV dysfunction can be due to noncontractile or hypocontractile segments that are viable but are chronically ischemic (hibernating myocardium). (AIIMS May 2011)
  2. As a consequence of chronic reduction in myocardial blood flow these segments down regulate their contractile function.
  3. These can be detected by using radionuclide scans of myocardial perfusion and metabolism, PET or delayed scanning with thallium-201; or by improvement of regional functional impairment, provoked by low-dose dobutamine.
  4. In such patients, revascularization improves myocardial blood flow, can return function, and can improve survival. (Ref. Hari. 18th ed., pg-2013)

Stress scintigraphy,

  1. When used in combination with the stress ECG, has yielded increased sensitivity (80%) and specificity (92%) over the standard stress ECG alone.
  2. Therefore, it is a particularly useful diagnostic tool when the standard stress ECG is expected to be of low yield (e.g., in patients with bundle branch block) and in patients in whom a previous stress ECG has produced equivocal results.
  3. Method. When the radioactive isotope thallium 201 (201TI) or the technetium-based isonitrile sestamibi is injected into the peripheral venous blood, the myocardial distribution of the substance is affected by blood flow and ischemia, with areas of less blood flow and ischemia taking up less 201TI or sestamibi than areas of normal blood flow. With exercise, blood flow increases, but in patients with coronary artery disease, those parts of the myocardium supplied by diseased coronary arteries and areas of MI take up less 201TI or sestamibi than normal areas. In patients who are unable to exercise, infusion of dobutamine (to increase oxygen demand) or dipyridamole or adenosine (to cause coronary vasodilation) are used to alter coronary flow. 

Stress echocardiography. Echocardiography can detect regional ischemia by identifying areas of wall motion abnormalities that occur with stress and are not present at rest. This regional dysfunction indicates that the area involved is not receiving adequate blood flow. The sensitivity is similar to radionucleotide imaging.


Cardiac catheterization with coronary arteriography allows for direct visualization of the coronary arteries by selective injection of radiographic contrast material. This procedure is the most sensitive and specific test commonly used for coronary artery disease.

Recent Advances
in Nuclear imaging

  1. Thallium scan          
  2. Technetium 99 scan             
  3. PET using N-13 NH3 or rubidium 82. 

Coronary angiography.


When assessed angiographically, flow in the culprit coronary artery is described by a simple qualitative scale called the thrombolysis in myocardial infarction (TIMI) grading system:



Grade 0 indicates complete occlusion of the infarct-related artery;



Grade 1 indicates some penetration of the contrast material beyond the point of obstruction but without perfusion of the distal coronary bed;



Grade 2 indicates perfusion of the entire infarct vessel into the distal bed but with flow that is delayed compared with that of a normal artery;



Grade 3 indicates full perfusion of the infarct vessel with normal flow.


  1. Oral Antiplatelet  (Ref. Hari. 18th ed., pg - 2019)
    1. Aspirin reduces mortality by 34%. (AIIMS Nov 2010)
    2. Prasugrel
    3. Clopidogrel
  2. Intravenous antiplatelet therapy
    1. Abciximab        
    2. Eptifibatide          
    3. Tirofiban
  3. Anticoagulant
    1. Unfractionated heparin (UFH)  
    2. Enoxaparin          
    3. Fondaparinux              
    4. Bivalirudin
  4. Beta blockers:
  5. Nitrates:
  6. Calcium antagonists: diltiazem (in Prinzmetal angina).
  7. Statin if total cholesterol is high
  8. K+ channel activator, eg Nicorandill
  9. Ranolazine – It is new anti anginal drug useful for refractory angina. (AIIMS May 2011)
    Ranolazine, use for patients with chronic angina who continue to be symptomatic despite a standard medical regimen. The mechanism – it inhibits the late inward sodium current (INa).
  10. Revascularization. 

Indication of revascularization & CABG (Ref. Hari. 18th ed., pg - 2013)

  1. Patients with an unacceptable level of angina despite optimal medical management should be considered for coronary revascularization.
  2. Patients with single- or two-vessel disease with normal LV function and anatomically suitable lesions ordinarily are advised to undergo PCI.
  3. Patients with three-vessel disease (or two-vessel disease that includes the proximal left descending coronary artery) and impaired global LV function (LV ejection fraction < 50%) or diabetes mellitus and those with left main coronary artery disease or other lesions unsuitable for catheter-based procedures should be considered for CABG as the initial method of revascularization. 
  1. Percutaneous transluminal coronary angioplasty (PTCA)
    1. Involves balloon dilatation of the stenotic vessel(s).
    2. Stenting reduces restenosis rates.
    3. Drug-coated stents reduce restenosis. Drug used are  a. Sirolimus (also known as Rapamycin) Q, b. Paclitaxel (MCQ)
    4. Antiplatelet agents, eg clopidogrel reduce the risk of stent thrombosis.
    5. IV platelet glycoprotein IIb/IIIa- inhibitor can reduce procedure-related ischemic events.
      Example: eptifibatide Q , tirofiban, abciximab
  2. Thrombolysis: Hemorrhage is the most frequent and potentially the most serious complication.

Recent Advances: Triflusal (New Drug)


Triflusal is a platelet aggregation inhibitor

Mechanism of action:


Triflusal is a platelet antiaggregant through;

  1. Blocks cyclooxygenase inhibiting thromboxane A2, preventing aggregation.
  2. 2, Preserves vascular prostacyclin, thus promoting anti-aggregant effect
  3. Blocks phosphodiesterase thereby increasing cAMP concentration, thereby promoting anti-aggregant effect due to inhibition of calcium mobilization 

Algorithm for risk stratification and treatment of patients with suspected CAD.

  1. Low risk patient having UA/NSTEMI. Early conservative therapy = Aspirin clopidogrel, anticoagulant, anti-ischemic therapy.
  2. High risk patient having UA/NSTEMI = Aspirin, anticoagulant, ADP inhibitor, (use IIb/IIIa inhibitor if unstable angina is there) anti-ischemic therapy, early invasive therapy.
  3. STEMI = Percutaneous coronary intervention (PCI), thrombolysis
    Anticoagulant are LMWH, Fondaparinux
    Anti-ischemic therapy = beta-blockers nitrate
    ADP antagonist = Clopidogrel or prasugrel. 

Recent Advances:


Black hole phenomena

  1. Restenosis remains an important issue even after coronary brachytherapy despite its efficacy in the treatment for in-stent restenosis.
  2. Vascular radiation was proposed as a therapy for restenosis prevention.
  3. Intracoronary radiation therapy and make it a safe, feasible, effective, and clinically useful tool to reduce restenosis.
  4. The acute and chronic changes in vascular wall are unique following brachytherapy.
  5. The restenotic tissue post coronary brachytherapy is relatively acellular and appears echolucent in intravascular ultrasound examination.
  6. This is dubbed the “black hole” phenomenon. Despite the similarity in the mode of action of brachytherapy and drug eluting stent implantation, the black hole phenomenon seems to be uncommon after drug-eluting stent implantation except in those patients who have had prior brachytherapy, bare-metal placement and after treatment of saphenous venous graft stenosis

Acute MI {Acute coronary syndrome (ACS)} (Ref. Hari. 18th ed., Pg-2021)


Definitions ACS includes unstable angina and evolving MI, which share a common underlying pathology-plaque rupture, thrombosis, and inflammation.


ACS may rarely be due to emboli or coronary spasm in normal coronary arteries, or vasculitis.


(Ref: Journal of the American College of Cardiology and AHA)


Table: Clinical classification of different types of myocardial infarction.

Type 1


Spontaneous myocardial infarction related to ischemia due to a primary coronary events such as plaque erosion and/or rupture, fissuring, or dissection.

Type 2


Myocardial infarction secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension.

Type 3


Sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by presumably new ST elevation, or new LBBB, evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood.

Type 4a


Myocardial infarction associated with PCI

Type 4b


Myocardial infarction associated with stent thrombosis as documented by angiography or at autopsy

Type 5

Myocardial infarction associated with CABG


The new ACC/ESC definition of myocardial infarction (MI)1


Definition of reinfarction


The definition of MI in patients undergo-ing CABG, The CK-MB threshold should be 5times the upper limit of normal and the CK-MB threshold for PCI should be 3 times the upper limit of normal.

Diagnosis is based on the presence of at least 2 out of 3 of (WHO criteria):

  1. Typical history         
  2. ECG: changes              
  3. Cardiac enzyme rise. 


  1. Acute central chest pain, lasting >20min, often associated with nausea sweating, dyspnea, palpitations. Ashen Grey Colour of the face is an important feature.
  2. May present without chest pain ('silent' infarct) in elderly or diabetics Q. In such patients, presentations may include: profuse sweating, syncope, pulmonary oedema, epigastric pain and vomiting, hypotension, oliguria, acute confusional state. 


  1. Sweating, pulse increase or decrease, BP increase or decrease.
  2. Bradycardia is seen in Inferior wall MI.
  3. There may be signs of heart failure raised JVP, 3rd & 4th heart sound Q and basal crepitation
  4. A pansystolic murmur Q (papillary muscle dysfunction/rupture, or VSD).
  5. A pericardial friction rub Q 

Arterial supply

  1. Anteroseptal  – Left anterior descending (LAD) (Most common site)
  2. Lateral wall         – Left circumflex
  3. Inferior wall       – Right coronary artery    (Second Most common site)

Important Points: LAD =  Widow’s artery (LQ 2012) 

  1. Ant wall MI findings seen in leads   - V1 – V6 , L1, AVL Q Artery involved left coronary artery
  2. Inf wall MI     - LII, LIII, AVF Q Artery involved right coronary artery
  3. Lat wall MI    - LI, AVL, V5, V6 Q Artery involved circumflex
  4. Antero septal = V1-3   Most common site, Artery involved LED. 


  1. ECG: Classically, hyperacute (tall) T waves (1st sign of MI in ECG)Q (LQ 2012) occurs within minutes of MI.
  2. ST elevation (Pardee’s)Q or occur within 2 –3 hours.
  3. T wave inversion occurs with in 8-12 hrs and development of pathological Q waves (transmural infarction) follow over 18-24 hours to days.
  4. In 10- 20% of cases of acute MI, the ECG may be normal initially Q!!!.
  5. Right coronary artery supply right ventricle, inferior wall of LV and posterior part of the interventricular septum. ECG is not a good tool to diagnose ischemia of the posterior part of interventricular septum. 

Serum cardiac markers –

Enzyme Begin Peak Normal
CPK MB 4 – 8 hr 16 – 32 hr 2 – 3 days
LDH 12 – 24 hr 48 – 60 hr 7 – 10 weeks


Extra Edge

  1. CPK – MB /  CPK- ratio of >2.5 is highly suggestive of MI.
  2. CPK MB also raised in
    1. Myocarditis
    2. Electrical cardioversion
    3. Cardiac surgery
  3. CPK MB has two isoforms
  4. CPK MB2/CPK MB1 >1.5 highly sensitive for MI Q
  5. Cardiac specific Troponin T/Troponin I (LQ 2012) are normally not detectable in the blood of healthy individuals but may increase after STEMI to levels >20 times higher than the upper level. So they are preferred biochemical markers for MI Q (Ref. Hari. 18th ed., pg -2023)
  6. Troponin T Test (TnT) – Becomes +ve with in 2 – 4 hr and remain elevated for upto 10 – 14 days. Troponin T is the best test to diagnosis acute MI. Only in cases of reinfarction within 2 weeks, CPK- MB is more useful than troponin T. 

Management of acute coronary syndrome (ACS)

  1. Aspirin 300mg chewed
  2. GTN sublingual.
  3. Analgesia Morphine 2-3 mg IV or 10 – 15 mg IM
  4. Thrombolysis, if no contraindication or primary angioplasty
  5. Beta-blocker
  6. ACE-inhibitor. Consider starting ACE-I (eg lisinopril 2.5mg) even in all normotensive patients within 24h of acute MI, especially if there is clinical evidence of heart failure or echo evidence of LV dysfunction.

Role of ACEI in acute MI

  1. To control BP
  2. To control LVF
  3. To help in the remodeling of infarct tissue. 
  1. Low molecular weight heparin (eg enoxaparin).
  2. GP IIb/ IIIa antagonist (eg tirofiban) used in High-risk patients (persistent or recurrent ischaemia, ST-depression, diabetes, raised troponin)
  3. Clopidogrel, in addition to aspirin, should be considered for up to 12 months.

Important Points:

  1. Warfarin is not used in treatment of Ac MI.
  2. Triflusal reduces thromboxane synthesis so prevents platelet aggregation. It is an alterative to aspirin in secondary prophylaxis of CVA and MI.
    (This is new drug. It is not given in Harrison 18th Edition !!!)
  3. Trimetazidine is controls myocardial ischemia through intracellular metabolic changes. It protect the heart from the deleterious effects of ischemia, and enhance LV contractility in patients with stunned or hibernating myocardium. (AIIMS Nov 2012)  
  4. Ticagrelor has been approved for the reduction of thrombotic events in patients with acute coronary syndrome. 

Recent advances in the management of MI

  1. Enhanced external counter pulsation (Ref. Hari. 18th ed., pg -2013)
    1. Enhanced external counterpulsation utilizes pneumatic cuffs on the lower extremities to provide diastolic augmentation and systolic unloading of blood pressure in order to decrease cardiac work and oxygen consumption while enhancing coronary blood flow.
    2. Regular application improves angina, exercise capacity, and regional myocardial perfusion.
  2. Trans myocardial LASER revascularization.
    1. Transmyocardial laser revascularization (to increase intramyocardial channels of blood flow), and the currently experimental approaches of gene and stem cell therapies are under study. (Ref. Hari. 18th ed., pg -1526)

Note: About Trans myocardial LASER revascularization, it is mentioned in 17th edition but it is not there in 18th edition !!!)


Newer Antianginal Drugs

  1. Metabolic modulators, eg, trimetazidine, ranolazine
  2. Direct bradycardic agents, eg, ivabradine
  3. Potassium channel activators, eg, nicorandil
  4. Rho-kinase inhibitors, eg, fasudil
  5. Protein kinase G facilitators, eg, detanonoate
  6. Sulfonylureas, eg, glibenclamide (This helps in myocardial ischemic preconditioning) 

Recent Advances: Ischemic preconditioning (IPC)

  1. In the heart, IPC is an intrinsic process whereby repeated short episodes of ischaemia protect the myocardium against a subsequent ischaemic insult. 
  2. If the blood supply to an organ or a tissue is impaired for a short time (usually less than five minutes) then restored so that blood flow is resumed, and the process repeated two or more times, the cells downstream of the tissue or organ are robustly protected from a final ischemic insult when the blood supply is cut off entirely and permanently.
  3. The protective effect which is imparted by IPC has two windows of protection. The first, lasts between 4–6 hours  and has been named classical or early preconditioning. The second window begins at 24 hours lasting up to 72 hours post the ischaemia and reperfusion stimulus. 


  1. The metabolic modulators are known as pFOX inhibitors because they partially inhibit the fatty acid oxidation pathway in myocardium.
  2. Because metabolism shifts to oxidation of fatty acids in ischemic myocardium, the oxygen requirement per unit of ATP produced increases.
  3. Partial inhibition of the enzyme required for fatty acid oxidation (long-chain 3-ketoacyl thiolase, LC-3KAT) appears to improve the metabolic status of ischemic tissue.


  1. The primary mechanism of therapeutic action of ranolazine involves reduced contractility.
  2. This action results from blockade of a late sodium current that facilitates calcium entry via the sodium-calcium exchanger.
  3. Ranolazine is approved for use in angina in the USA.


  1. It is called as bradycardic drugs, relatively selective If sodium channel blockers, reduce cardiac rate by inhibiting the hyperpolarization-activated sodium channel in the sinoatrial node.
  2. No other significant hemodynamic effects occurs.
  3. Ivabradine appears to reduce anginal attacks with an efficacy similar to that of calcium channel blockers and beta blockers.
  4. The lack of effect on gastrointestinal and bronchial smooth muscle is an advantage of ivabradine.
  5. Ivabradine acts by reducing the heart rate in a mechanism different from beta blockers and calcium channel blockers, two commonly prescribed antianginal drugs.
  6. It is classified as a cardiotonic agent
Adverse effects
Luminous Phenomena (by patients described as sensations of enhanced brightness in a fully maintained visual field).

Fasudil Hydrochloride


It is a potent Rho-kinase inhibitor and vasodilator. 

It is used for the treatment of cerebral vasospasm, which is often due to subarachnoid hemorrhage, as well as to improve the cognitive decline seen in stroke victims. It is effective for the treatment of pulmonary hypertension. 

It is used to enhance memory and improve the prognosis of Alzheimers patients



  1. It has vasodilating properties in normal coronary arteries.
  2. It reduces both preload and afterload.
  3. It also provides some myocardial protection via preconditioning by activation of cardiac KATP channels.
  4. It significant reduction in relative risk of fatal and nonfatal coronary events in patients receiving the drug. 

RV infarct



  1. Usually associated with inferior wall MI
  2. JVP is raised Q
  3. Kussmaul sign is positive Q
    1. Catheterization of the right side of the heart often reveals a distinctive hemodynamic pattern resembling constrictive pericarditis (steep right atrial "y" descent and an early diastolic dip and plateau in RV waveforms) (Ref. Hari. 18th ed., pg - 2032)
    2. Patient may or may not have hypotension Q
    3. Right ventricular failure (RVF)/infarction: Presents with low cardiac out and JVP raised. Do a Swan-Ganz catheter to measure right -sided pressures a guide fluid replacement Q
    4. Give IV fluid for hypotension Q

Unstable angina: Manage along standard lines but thrombolysis is not done.


Important Points: - CABG


Indications for CABG (to improve survival)

  1. Left mainstem disease
  2. Triple vessel disease involving proximal part of the left anterior descending.

To relieve symptoms

  1. Angina unresponsive to drugs
  2. Unstable angina (sometimes)
  3. If angioplasty is unsuccessful

NB: When CABG and PTCA are both clinically valid options, PTCA is preferred.

  1. Artery used for by pass graft
    1. Internal mammary artery                
    2. Radial artery
  2. Vein used for by pass graft
    1. Long saphenous vein
    2. Mortality 50% of deaths occur within 24h of onset of symptom. (MCQ)
Complications of MI
  1. Bradycardia or heart block:
    1. Sinus bradycardia: treat with atropine Q 0.6 -1.2mg, or injection isoprenaline
      Consider temporary cardiac pacing if no response, or poorly tolerated by the patient. 
    2. 1st degree AV block: Observe closely as approximately 40% develop higher degrees of AV block.
    3. 2nd degree (II A block) Wenckebach (Mobitz type I) block: Does not require pacing Q.
    4. 2nd degree (II B block) Mobitz type II block: Carries a high risk of developing complete AV block; should be paced Q.
    5. Complete AV block: insert pacemaker
    6. Bundle branch block: MI complicated by trifascicular block or non-adjacent bifascicular disease should be paced.
  2. Tachyarrhythmias:
    1. K+, hypoxia and acidosis Q all predispose to arrhythmias and should be corrected.
    2. Regular broad complex tachycardia after MI is almost always VT.
    3. If hemodynamically stable, treat with antidysrhythmic.
    4. Early VT: give lidocaine by infusion for 12-24h or amiodarone.
    5. Late VT (>24h) amiodarone and start oral therapy (amiodarone or sotalol)
    6. If hemodynamically compromised give DC shock.
    7. Af or flutter If hemodynamically compromised, DC cardioversion Otherwise control rate with digoxin or  beta -blocker.
    8. In atrial flutter or intermittent Af, give amio­darone or sotalol. 

In MI, Bradycardia is most common in inferior wall MI. (LQ 2012) &  Tachyarrhythmias are most common in anterior wall MI. (LQ 2012)


Important Points:


Dofetilide: It is a pure K+ channel blocker, used for maintenance of sinus rhythm in symptomatic atrial flutter and fibrillation. It increase the refractory period of both atria and ventricles.

  1. Left ventricular failure (LVF)
    Killip’s classification (for assessing the prognosis of a case of MI. It is based on degree of LV dysfunction)
    (Note: With the recent advancement in treatment of MI, the above mentioned mortality percentage is much reduced now) 
  2. Cardiogenic shock –  By definition
    1. Systolic arterial pressure < 90 mmHg
    2. Cardiac index < 1.8 L/min/m2
    3. Pulm capillary wedge pressure >18 mm Hg

      Treatment –
    4. Vasopressor – Dopamine, Dobutamine, Amrinone Milrinone
    5. Intra aortic balloon pumping (IABP)
    6. PTCA (It is the treatment of choice) MCQ (AIPG 12) 
  1. Right ventricular / infarction: Presents with low cardiac out and JVP raised (LQ 2012). Do a Swan-Ganz catheter to measure right -sided pressures a guide fluid replacement Q (LQ 2012)
  2. Pericarditis: Central chest pain, relieved by sitting forwards. ECG: saddle-shaped ST elevation Q
    Treatment-: NSAIDS. Echo to check for effusion.
  3. DVT & PE: Patients are at risk of developing DVT & PE and should be prophylactically heparinized Q (enoxaparin) until fully mobile.
  4. Systemic embolism: May arise from a LV mural thrombus. After large anterior MI, consider anticoagulation with warfarin Q for 3 months.
  5. Mitral regurgitation: Occurs due to papillary muscle dysfunction Q
  6. Ventricular septal defect: Presents with pansystolic murmur Q, JVP raised Q, cardiac failure Q.
    Diagnosis: Echo.
    Treatment: Surgery.
  7. Free wall rupture – with in first week
    1. Usually seen in first infarction, HT, no h/o angina and large Q wave infarct.
    2. Presents with sudden loss of pulse, blood pressure & loss of consciousness. Electro mechanical dissociation occurs Q . Electrical alternans is seen. Q
    3. Cardiac tamponade result Q
  8. Late malignant ventricular arrhythmias: Occur 1-3wks post-MI. Avoid hypokaliemia the most easily avoidable cause. Consider 24h ECG monitoring prior to discharge if large MI.
  9. Dressler's syndrome: Recurrent pericarditis, pleural effusions, fever, pain chest Q, anaemia and raised ESR 2-3 months post-MI.
    Treatment: NSAIDS; steroids if severe.
  10. Left ventricular aneurysm: This occurs late (4-6wks post-MI), and presents with LVF, angina. recurrent VT or systemic embolism.
    ECG: Persistent ST segment elevation Q.
  11. Shoulder hand syndrome = Pain In the shoulder joints occur after 2-3 months.

Test Your Skills Now!
Take a Quiz now
Reviewer Name