cardio

Question 1

Types of MI

Answer 1

Type 1- Infarction due to coronary atherothrombosis

Type 2- Infarction due to supply-demand mismatch that is not the result of acute atherothrombosis.

Type 3- Infarction causing sudden death without the opportunity for biomarker or ECG confirmation.

Type 4a- Infarction related to a percutaneous coronary intervention.

Type 4b- Infarction related to the thrombosis of coronary stent.

Type 5- Infarction due to CABG.

Question 2

Acute renal failure after cardiac catheterization

Answer 2

Think of contrast nephropathy and renal atheroemboli

Cholesterol emboli:
the presence of other signs of embolization such as blue toes, livedo reticularis, Hollenhorst plaque in the retina and abdominal pain.
transient eosinophilia and hypocomplementemia
persistent renal failure after seven days.

Contrast nephropathy:
risk greatest in moderate to severe renal insufficiency and diabetes.
plasma creatinine concentration returns to baseline within seven days
to prevent this, use iso-osmolar agents in patients with CKD.

Question 3

Features of complete heart block

Answer 3

• syncope
• heart failure
• regular bradycardia (30-50 bpm)
• wide pulse pressure
• JVP: cannon waves in neck
• variable intensity of S1

Question 4

jvp

Answer 4

‘a’ wave = atrial contraction ( a for atrial)

• large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
• absent if in atrial fibrillation

Cannon ‘a’ waves

• caused by atrial contractions against a closed tricuspid valve
• are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single chamber ventricular pacing

‘c’ wave (c for closure)

• closure of tricuspid valve
• not normally visible

‘v’ wave (v for volume filling)

• due to passive filling of blood into the atrium against a closed tricuspid valve
• giant v waves in tricuspid regurgitation

‘x’ descent = fall in atrial pressure during ventricular systole

‘y’ descent = opening of tricuspid valve

Question 5

mitral stenosis

Answer 5

Examination findings in MS:
– reduced arterial pulse volume.
– prominent “a” wave in JVP.Absent in AF.
– prominent “v” wave secondary to TR.
– right ventricular heave
– palpable S2.
– loud S1.
– late diastolic murmur in mild MS, early diastolic murmur in severe MS.

Specific signs of severe MS:
– mitral facies (pinkish purple patches on cheeks)
– Prominent V wave in the jugular venous pressure
– right ventricular lift
– early opening snap following S2.
– loud pulmonary component of the second heart sound
– early diastolic murmur
(murmur diminished in Inspiration, augments with Expiration)

Other murmurs or sound when pulmonary hypertension is present:
– pulmonary ejection sound
– holosystolic murmur of TR heard best along right sternal border which increases with Inspiration
– Graham Steel murmur of Pulmonary Regurgitation best heard at the base.

Question 6

Surgery is indicated in patient with moderate to severe MS in the following settings

Answer 6

Among patients who are symptomatic(NYHA class III-IV) if:

1) Percutaneous mitral balloon valvotomy is not available.
2) PMBV is contraindicated because of moderate to severe MR or of left atrial thrombus that persists despite anticoagulation.
3) Mitral valve morphology is not favourable for PMBV in patients with acceptable operative risk.

Symptomatic patients who also have moderate to severe MR.

Question 7

Contraindications to PMBV

Answer 7

1) Mitral valve area >1.5cm2
2) Left atrial thrombus
3) Moderate to severe MR
4) Severe or bicommissural calcification
5) Absence of commisural fusion
6) Severe concomitant aortic valve disease,or severe combined tricuspid stenosis and regurgitation.
7) Concomitant CAD requiring bypass surgery.

If any of the following is present, proceed with surgery preferably mitral valve repair.

Question 8

murmurs

Answer 8

Systolic Murmur:
Early systolic- MR, TR, VSD
Midsystolic ejection- Aortic stenosis, Aortic sclerosis.
Holo/Pansystolic – MR, TR, VSD
Late systolic- Mitral valve prolapse, Tricuspid valve prolapse

Diastolic murmur:
Early diastolic – AR, PR
Mid-diastolic- MS, TS, Atrial myxoma
Late diastolic- MS, TS, Atrial myxoma, Complete heart block.

Practical Tip:
rIght sided murmur louder on Inspiration
lEft sided murmur louder on Expiration

Question 9

ICD placement IN HOCM

Answer 9

indicated if any ONE of the major risk factors are present:

1) Left ventricular wall thickness >30 mm
2) Family history of premature sudden cardiac death
3) Previous cardiac arrest/ventricular tachycardia
4) Previous episodes of documented non-sustained VT (>3 beats, rate >120 bpm)
5) Unexplained syncope

Question 10

Drugs to avoid in CHF

Answer 10

• anti-arrhythmic agents (apart from beta-blockers and amiodarone)
• non-dihydropyridine calcium-channel blockers (verapamil, diltiazem)
• tricyclic antidepressants
• non-steroidal anti-infl ammatory drugs and COX-2 inhibitors
• clozapine
• metformin and thiazolidinediones(pioglitazone, rosiglitazone)
• corticosteroids (glucocorticoids and mineralocorticoids)
• tumour necrosis factor antagonist biologicals.

Question 11

HASBLED score

Answer 11

Hypertension
Abnormal renal and liver function
Stroke
Bleeding
Labile INR
Elderly
Drugs or alcohol

1 pt each
≥3 indicates “high risk”

Question 12

CHF drugs not shown to improve survival

Answer 12

No improvement in survival/mortality

1) Diuretics
2) Digoxin
3) Amlodipine
4) Felodipine

Question 13

NYHA

Answer 13

Class I (Asymptomatic): No limitations in normal physical activity

Class II (Mild): Slight limitation of physical activity. Ordinary physical activity results in fatigue, palpitation, dyspnoea or angina pectoris

Class III (Moderate): Marked limitation of physical activity. Less than ordinary activity results in symptoms

Class IV (Severe): Unable to carry our any physical activity without discomfort. Symptoms present at rest

Question 14

HOCM mx

Answer 14

Useful:

• beta blockers-ameliorate angina and syncope
• amiodarone-reduce frequency of supra ventricular
• non-dihydropyridine ca blocker-reduce the stiffness of the left ventricle, reduce the elevated diastolic pressures, increase exercise tolerance, and, in some instances, reduce the severity of outflow tract pressure gradients.
• disopyramide- reduce LV contractility

Not useful:
Digitalis, diuretics, nitrates, dihydropyridine calcium blockers, vasodilators,and beta-adrenergic agonists are best avoided, particularly in patients with known LV outflow tract pressure gradients.

Alcohol ingestion may produce sufficient vasodilatation to exacerbate an outflow pressure gradient.

Question 15

dissection of the ascending aorta

Answer 15

1) Acute myocardial ischaemia or MI due to coronary occlusion.RCA most commonly involved.
2) Diastolic decrescendo murmur,hypotension and heart failure due to Acute aortic insufficiency
3) Murmur best heard along RIGHT sternal border.
4) Cardiac tamponade and sudden death
5) Hemothorax
6) A considerable variation >20mmmHg in systolic BP between the arms.
7) Neurological deficit including stroke or decreased LOC.
8) Horner’s syndrome
9) Vocal cord paralysis and hoarseness.

Classification of aortic dissection based on the Daily system:

1) Type A- dissection that involves the ascending aorta.
2) Type B- all other dissections.

AVOID
Hydralazine should be avoided as they increase shear stress and provide less accurate and reversible control of blood pressure.

For BP control
-iv labetalol - if Bp >100 –> sodium nitroprusside

Question 16

acceptable normal variants in a young athelete

Answer 16

1) Bradycardia
2) Wenkebach
3) Junctional rhythm
4) First degree heart block
5) RBBB

Question 17

AF VTE Risks

Answer 17

Major risk factors include the following:

1) Previous stroke or TIA
2) Age >75 years.
3) Presence of valvular heart disease (Mitral stenosis or prosthetic heart valves)

The others: HT, diabetes, dyslipidemia, Age 65-74 are non major risk factors.

Question 18

Indications for Pacing (Permanent pacemaker implantation):

Answer 18

• Symptomatic Sinus node dysfunction (SND)
• Acquired AV blocks in adults- Advanced 2nd degree (Mobitz Type II) or 3rd degree heart block (symptomatic/asymptomatic)
• Chronic bifascicular block- Advanced 2nd degree block(Mobitz Type II) or intermittent 3rd degree block or alternating bundle branch block.
• Persistent and symptomatic 2nd or 3rd degree AV block after STEMI.
• Symptomatic Hypersensitive carotid sinus syndrome and neurocardiogenic syncope
• Persistent inappropriate or symptomatic bradycardia not expected to resolve after cardiac transplantation
• Sustained pause dependent VT with or without QT prolongation.

Question 19

Indications for biventricular pacemaker-defibrillator placement:

Answer 19

1) NYHA class III or IV heart failure,
2) ejection fraction less than or equal to 35%
3) QRS width greater than 120 msec.

Approximately 70% of patients who undergo biventricular device placement obtain a symptomatic benefit, thought to result from mechanical resynchronization of the timing of right and left ventricular contraction.

These devices have been shown to improve ejection fraction, quality of life, and functional status, as well as to decrease heart failure hospitalizations and mortality.
Amiodarone does not improve symptoms of heart failure or decrease mortality

An ICD will only reduce the risk of sudden death but will not help ameliorate his symptoms.

A dual-chamber (atrioventricular) pacemaker-defibrillator will only provide additional protection from sinus bradycardia by atrial pacing but will not reduce his risk of sudden death.

CONCLUSIONS: Among patients with NYHA class II or III heart failure, a wide QRS complex, and left ventricular systolic dysfunction, the addition of CRT to an ICD reduced rates of death and hospitalization for heart failure. This improvement was accompanied by more adverse events.

Question 20

ppm indication after MI

Answer 20

Permanent Pacing indicated in:

• Persistent/transient 2nd degree AV block or 3rd degree block and associated bundle branch block
• Persistent and symptomatic 2nd or 3rd degree AV block.

Permanent Pacing NOT indicated in:

• Transient AV block in absence of intraventricular conduction defects.
• Transient AV block in presence of isolated left anterior fascicular block.
• New bundle branch block in absence of AV block.
• Persistent asymptomic 1st degree AV block in presence of bundle branch or fascicular block.

Question 21

benefits of cardiac resynchronization

Answer 21

1) Improvement in 6 minute walking distance
2) Improvement in quality of life
3) Improvement in VO2 max
4) Improvement in hospitalization for heart failure
5) Reduction in NYHA class score
6) Decreased mortality

Question 22

torsades

Answer 22

Antiarrhythmic drugs to avoid in Torsades:

1) class IA agents (eg, quinidine, procainamide, disopyramide),
2) class IC agents (eg,flecainide),
3) class III agents (eg, sotalol, amiodarone).

Treatment:

1) Correct underlying cause.ie: electrolyte disturbance
2) Magnesium sulphate
3) Consider overdrive pacing or isoproterenol infusion

4) Consider DC cardioversion if hemodynamically unstable.

Question 23

level of blockade @ heart block

Answer 23

Mobitz I heart block is characterized by progressive prolongation of the PR interval on the electrocardiogram (ECG) on consecutive beats followed by a blocked P wave (i.e., a ‘dropped’ QRS complex). After the dropped QRS complex, the PR interval resets and the cycle repeats.

It is almost always a disease of the AV node.

Mobitz I is usually due to reversible conduction block at the level of the AV node. Malfunctioning AV node cells tend to progressively fatigue until they fail to conduct an impulse.

This is in contrast to Mobitz II block where the cells of the His-Purkinje system tends to fail suddenly and unexpectedly.

Question 24

INTERHEART study

Answer 24

According to the INTERHEART study, published in Lancet in 2004, up to 49% of all population attributable risk(PAR) of first MI was due to dyslipidemia.

Findings of the INTERHEART study:

• Raised ApoB/ApoA1 ratio PAR 49.2%
• Smoking PAR 35.7%
• Psychosocial factors PAR 32.5%
• Abdominal obesity PAR 20.1%
• Hypertension 17.9%
• Lack of daily consumption of fruits and vegetables PAR 13.7%
• Lack of regular physical activity PAR 12.2%
• Diabetes PAR 9.9%
• Regular alcohol consumption PAR 6.7%

Question 25

Contraindications to EST

Answer 25

- LBBB - Severe HOCM - Severe AS - Recent AMI (3-4 days) - Unstable angina with recent rest pain or increased symptoms. - Untreated life threatening cardiac arrhythmia - Advanced AV block - Uncontrolled systemic HT (>220/120) - Acute systemic illness ie: PE, aortic dissection - Unable to perform test ie: gait disturbance,severe OA.

Question 26

Commotio cordis

Answer 26

Commotio cordis occurs due to a blunt force injury to the chest wall that results in an often fatal arrhythmia, most frequently ventricular fibrillation. In animal studies, commotio cordis has been found to occur when the blunt force is applied at 20-50 mph and only during specific timing within the cardiac cycle (C Madias et al: J Cardiovasc Electrophysiol 18:115, 2007; MS Link et al: N Engl J Med 338:1805, 1998). If the force were delivered during the upstroke of the T wave (10-30 msec before the peak), ventricular fibrillation would frequently result. If the force were applied during the QRS (depolarization), transient complete heart block might occur (MS Link et al: N Engl J Med 338:1805, 1998). In reported case series, the survival of commotio cordis is only 15%. Defibrillation is most successful if applied within 3 min.

Question 27

Congenital long QT syndrome (LQTS)

Answer 27

– recurrent syncope triggered by activity, – Corrected QT intervals are considered abnormal if greater than 440 msec in men and 450 to 460 msec in women, but there is substantial overlap among normal patients and abnormal LQT gene carriers. – QTc >500 represents greatest risk of symptomatic arrhythmias. – family history of early sudden death. – Cardiac events in LQTS patients include syncope and cardiac arrest due to torsade de pointes ventricular tachycardia. – Ninety percent of congenital LQTS cases are caused by mutations in three genes, and triggers of events vary by genotype. – The risk of a cardiac event in LQTS is related to age, sex, QTc interval, genotype, and specific mutation. – β-Blockers are most protective in LQTS type 1 patients, as compared to those with LQTS type 2 or type 3. – All patients with congenital LQTS should be treated with a β-blocker, regardless of symptoms. – Patients with recurrent syncope or cardiac arrest on β-blockers are candidates for defibrillator placement. LQTS type 1 (most common): – Caused by mutations in KCNQ1, the α subunit of the delayed rectifier potassium channel (IKs). – LQTS type 1 patients experience the majority of their events during exercise. – Events during swimming may be specific for LQT1 mutations. LQTS type 2 – caused by mutations in the KCNH2/HERG gene, which codes for IKr, the rapid component of the delayed rectifier potassium channel. – Events usually precipitated by emotional arousal, exercise, or loud or sudden noises. LQTS type 3 – caused by gain-of-function mutations in the sodium channel gene (SCN5A). – The QT interval is usually quite prolonged, and events often occur during sleep.

Question 28

Brugada syndrome

Answer 28

– Autosomal dominant – Peak prevalence of SCD in 4th decade – Characterized by a pseudo right bundle branch block pattern with ST-segment elevation on the electrocardiogram and ventricular arrhythmias. – ECG changes may be elicited with flecainide challenge – Loss-of-function mutations in the SCN5A gene are present in approximately 30% of patients.

Question 29

short QT synd

Answer 29

– carries a high risk of sudden cardiac death. – autosomal dominant – short QT interval – atrial fibrillation occurring at a young age – increased risk of death due to ventricular fibrillation.

Question 30

WPW

Answer 30

– characterized by ventricular preexcitation (short PR interval and delta wave) and symptomatic tachycardia. – Owing to the rapid conduction properties of some accessory pathways, atrial fibrillation can be a life-threatening arrhythmia in these patients due to rapidly conducting atrial fibrillation degenerating to ventricular fibrillation. – Although patients with Wolff-Parkinson-White syndrome have an increased risk of sudden cardiac death, it is very unusual for this to be the first symptomatic manifestation of the syndrome.

Question 31

Arrhythmogenic right ventricular dysplasia

Answer 31

– autosomal dominant – fibro-fatty infiltration of right ventricle leading to poor right ventricular function with preserved left ventricular function. – May be diagnosed by cardiac MRI (Fatty infiltration of the RV free wall can be visible on cardiac MRI) – Right ventricular angiography is considered the gold standard for the diagnosis of ARVD. Findings consistent with ARVD are an akinetic or dyskinetic bulging localized to the infundibular, apical, and subtricuspid regions of the RV. The specificity is 90% – leading cause of SCD in young adults Italy – May have either LBBB or RBBB but most common ECG abnormality seen in ARVD is T wave inversion in leads V1 to V3. Diagnostic Criteria: There is no pathognomonic feature of ARVD. The diagnosis of ARVD is based on a combination of major and minor criteria. - requires either 2 major criteria or 1 major and 2 minor criteria or 4 minor criteria. ``` Major Criteria: 1. Right ventricular dysfunction o Severe dilatation and reduction of RV ejection fraction with little or no LV impairment o Localized RV aneurysms o Severe segmental dilatation of the RV ``` 2. Tissue characterization o Fibrofatty replacement of myocardium on endomyocardial biopsy 3. Conduction abnormalities o Epsilon waves in V1 – V3. o Localized prolongation (>110 ms) of QRS in V1 – V3 4. Family history o Familial disease confirmed on autopsy or surgery ``` Minor Criteria 1. Right ventricular dysfunction o Mild global RV dilatation and/or reduced ejection fraction with normal LV. o Mild segmental dilatation of the RV o Regional RV hypokinesis ``` 2. Tissue characterization 3. Conduction abnormalities o Inverted T waves in V2 and V3 in an individual over 12 years old, in the absence of a right bundle branch block (RBBB) o Late potentials on signal averaged EKG. o Ventricular tachycardia with a left bundle branch block (LBBB) morphology o Frequent PVCs (> 1000 PVCs / 24 hours) 4. Family history o Family history of sudden cardiac death before age 35 o Family history of ARVD

Question 32

HOCM

Answer 32

– Autosomal dominant – Mutation mainly in cardiac β-myosin heavy chain. – Clinically presents with chest pain, exertional intolerance,syncope and arrhythmias. – Commonest cause of SCD age – ECHO shows LVH. Septal, Concentric, Apical, LV free wall and RV hypertrophy. – Beta blocker is mainstay of treatment- improves diastolic filling and prevents sudden death – Major risk factors for SCD in HOCM: Left ventricular wall thickness >30mm,Family history of premature SCD – Avoid Digoxin and diuretics (Increases obstruction) – Screen first degree relatives – Poor prognosis if abnormal response to blood pressure on exercise (ie: BP reduces with exercise)

Question 33

Hormones

Answer 33

Antiproliferative, vasodilation and Na/H20 excretion by: - ANP - BNP - Nitric oxide - Bradykinin Growth promotion, vasocontriction, Na/H20 retention by: - Angiotensin 2 - Aldosterone - Endothelia - Noradrenaline

Question 34

Diastolic heart failure

Answer 34

– stiffening of the ventricle, – commonest in elderly females Causes includes: 1) hypertension (most common) 2) Hypertrophic cardiomyopathy 3) Ischaemia 4) Infiltration Treatment 1) avoid fluid depletion and inotropes (including digoxin) 2) improve relaxation with beta blockers and calcium channel blocker 3) rate control of AF

Question 35

Beta blockers in heart failure

Answer 35

– improvement in mortality and morbidity in Class 2-4 (and class 1 post MI) – class 4 must be stabilized and euvolemic before initiation – carvedilol and slow release metoprolol are RCT proven – reduction in sudden cardiac death as well as HF death.

Question 36

Criteria for ICD as primary prevention in low EF heart failure

Answer 36

1) ICD in ALL mild to moderate heart failure with EF < 35% despite optimal medical therapy. 2) In Class 1 IHD if: – MORE than 40 days post AMI. – EF measured more than 3 months post revascularisation – Add cardiac resynchronisation therapy if QRS wide, class 3 or 4.

Question 37

hypertrophic cardiomyopathy

Answer 37

ICD

Question 38

anti-platelet therapy should be STOPPED prior to the following surgery:

Answer 38

1) Extraocular surgery, mainly strabismus and oculo-plastic surgery 2) Intracranial neurosurgery: ASA has been implicated in increased risk of postoperative intracerebral haematoma contributing to fatal outcome in some cases. 3) Spinal surgery: The consequences of bleeding into the closed spinal canal can result in irreversible cord damage. 4) TURP 5) Major reconstructive surgery For these operations, patients at low risk of stent thrombosis should have their antiplatelet therapy routinely ceased perioperatively Stopping dual anti-platelet therapy 5 days before surgery is adequate to prevent bleeding complications.Antiplatelet therapy should be recommenced as soon as possible after the procedure.

Question 39

Familial Hypercholesterolemia

Answer 39

Index cases of Familial Hypercholesterolemia present with one or more of the following features: 1) Severe hypercholesterolaemia that is not explained by secondary causes, 2) A strong personal or family history of premature atherosclerotic cardiovascular disease (CVD) 3) Tendon Xanthomas Cholesterol-lowering treatment such as the statin class of drugs provides excellent control of inherited high cholesterol levels. The statins work by reducing cholesterol synthesis in the liver. This stimulates SREBP and LDL receptor gene expression. As a result, the receptors produced by the normal gene will reduce LDL cholesterol levels. The effect of statins can be enhanced by bile acid sequestrants or cholesterol absorption inhibitors such as plant sterols or ezetimibe

Question 40

DES

Answer 40

decreased rates of target lesion revascularization and restenosis compared with bare metal stents. However, drug-eluting stents appear to increase the risk of late stent thrombosis compared to bare metal stents. Risk factors for late stent thrombosis with DES: – Discontinuation of dual antiplatelet therapy – longer stent length with DES – Incomplete stent apposition – resistance to antiplatelet therapy and heightened platelet reactivity Prevention of Late Stent Thrombosis: Dual antiplatelet therapy with aspirin and clopidogrel following stent implantation is recommended for at least: – four weeks to prevent stent thrombosis with BMS – three months with sirolimus-eluting stent – six months with paclitaxel-eluting stents

Question 41

Familial lipid disorders

Answer 41

Familial lipid disorders can be divided into 3 groups: 1) Triglyceride 2) LDL 3) HDL ``` Triglycerides: 1) Familial hypertriglyceridemia Clues to diagnosis: – pancreatitis – retinal vein thrombosis ``` 2) Lipoprotein lipase deficiency. Clues to diagnosis: – presents in childhood with eruptive xanthomas, lipaemia retinalis. – TG does NOT improve after FFP 3) Apoprotein C deficiency: Clues to diagnosis: – TG improves after FFP. First line treatment for Hypertriglyceridemia is Fibrates. ``` LDL: 1) Heterozygous familial hypercholesterolemia. Clues to dianosis: – typical family history of early CVD. – tendon xanthomas. – genetic defect is LDL receptor. ``` 2) Homozygous familial hypercholesterolemia-rare 3) Apoprotein B100 gene mutation 4) Polygenic hypercholesterolemia First line treatment is with statins +/- ezetimibe. HDL – Tangier disease- due to ABC1 gene mutation. First line treatment is fibrates.

Question 42

The AHA/ACC guideline recommends temporary bradycardia pacing in the following situations in patients with acute myocardial infarction

Answer 42

1) Asystole 2) Symptomatic bradycardia due to sinus node dysfunction or Mobitz type 1 second degree HB not responsive to atropine. 3) Mobitz type II second degree or complete heart block. 4) Bilateral or alternating bundle branch block. 5) A new BBB with first degree block 6) An old BBB with first degree block and a new fascicular block.