Saturday Clinical Meeting
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Saturday Clinical Meeting

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a case of HOCM

a case of HOCM

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Saturday Clinical Meeting Saturday Clinical Meeting Presentation Transcript

  • SATURDAY CLINICAL MEETING DEPARTMENT OF CARDIOLOGY 12 TH FEB 2005
  • DETAILS OF THE CASE
    • 40 years old serving soldier
    • Resident of Rourkela
    • Non-smoker, non-diabetic, non-hypertensive
    • Referred from CH(NC)
    • Date of admission – 24 Jan 2005
    • Informant – self
    • Reliability - good
  • PRESENTING COMPLAINTS
    • Syncope
    • Angina on exertion NYHA – III
    • Dyspnoea on exertion NYHA – III
    6months
  • WHAT IS SYNCOPE ?
  • SYNCOPE
    • A transient loss of consciousness
    • Spontaneous and full recovery
    • Loss of postural tone
    • No prolonged confusion
  • Discord in the Evaluation of Syncope Neurologist Cardiologist
  • SYNCOPE: CARDIAC ETIOLOGY
    • OBSTRUCTION TO FLOW (3-11%)
      • HOCM, AS, MS, myxoma
      • PS, PE, Pulm HTN
      • Tamponade
    • ARRHYTHMIAS (5-30%)
      • Sick sinus, AV block
      • VT, SVT
  • SYNCOPE: NONCARDIAC
    • Vasodepressor (1-29%)
    • Situational (1-8%)
    • Seizure
    • Psychogenic
    • Orthostatic (4-12%)
    • Drug-induced (2-9%)
    • Carotid sinus
    • Neuralgia
    • Neurologic (TIA, stroke, migraine)
  • HOW TO DISTINGUISH SEIZURES FROM SYNCOPE ?
  • - + POST-ICTAL HEADACHE - + POST-ICTAL AMNESIA - + POST-ICTAL CONFUSION - + TONGUE-BITE - + CYANOSIS - + AURA SYNCOPE SEIZURE
  • WHAT ARE THE CAUSES OF CHEST PAIN WITH SYNCOPE ?
  • LOSS OF BLOOD UPPER GE BLEED HYPOVOLEMIA DUE TO CHEMICAL PERITOITIS, SEVERE PAIN ACUTE PANCREATITIS CARDIORESPIRATORY EMBARRASSMENT PLEURAL HEMORRHAGE CARDIORESPIRATORY EMBARRASSMENT TENSION PNEUMOTHORAX CARDIAC COMPRESSION PERICARDIAL TAMPONADE OBSTRUCTION TO CIRCULATION ACUTE PULMONARY EMBOLISM LARGE AREA OF MYOCARDIUM AT RISK, ARRHYTHMIAS ANGINA PECTORIS ARRHYTHMIAS(VT/VF) VASOSPASTIC ANGINA LARGE AREA OF MYOCARDIUM AT RISK, ARRHYTHMIAS ACUTE MYOCARDIAL INFARCTION MECHANISM CONDITION
  • HISTORY
    • First episode of loss of consciousness while running in August 2004
    • Duration : 2-3 seconds
    • Preceded by angina
    • Similar episodes since last 6 months
    • No associated h/o
    • Palpitations
    • Sphincter incontinence/tongue bite
    • Patient presented with retrosternal discomfort associated with breathlessness initially during unaccustomed exercise which progressed to discomfort while doing routine activities
  • WHAT IS THE MECHANISM OF ANGINA IN HOCM ?
  • ARRHYTHMIAS INCREASED CORONARY VASCULAR RESISTANCE LEFT VENTRICULAR OUTFLOW OBSTRUCTION MYOCARDIAL BRIDGES MYOCYTE DISARRAY ABNORMAL VASCULAR RESPONSES DIASTOLIC DYSFUNCTION SMALL VESSEL DISEASE MYOCARDIAL HYPERTROPHY REDUCED MYOCARDIAL PERFUSION INCREASED MYOCARDIAL OXYGEN DEMAND
    • PAST HISTORY :
    • Not significant
    • FAMILY HISTORY :
    • No h/o sudden cardiac death
    • No h/o premature death
  • TREATMENT HISTORY
    • Tab Atenolol 100mg 01 OD
    • Tab Isoptin 40mg 01 TDS
    • Symptomatic improvement with medication
  • SUMMARY ON HISTORY
    • 40 years old serving soldier
    • No modifiable risk factors
    • No family h/o SCD
    • Presented with c/o syncope, AOE / DOE III
  • CLINICAL EXAMINATION
    • Height 166cms
    • Weight 68.9 Kgs
    • Average built
    • Pulse 80/min, regular, bisferiens, no radio-radial or radio-femoral delay
    • BP 130/90 mmHg
  • WHAT IS MEANT BY BISFERIENS PULSE ?
    • BIS means twice
    • FERIENS means beating
    • It is a double-peaked arterial pulse, so there is a mid-systolic dip
    • Both tidal and percussion wave are appreciable
  • WHAT ARE THE CAUSES OF BISFERIENS PULSE?
    • Severe aortic regurgitation
    • Aortic stenosis and regurgitation
    • Hypertrophic obstructive cardiomyopathy
    • Hyperkinetic circulatory states
    • Muscular exercise
  • GENERAL EXAMINATION
    • Fever (-)
    • Pallor (-)
    • Cyanosis (-)
    • Clubbing (-)
    • Jugular venous pulse ‘ a ’ wave prominent
    • Lymphadenopathy (-)
  • WHAT ARE THE CHANGES SEEN IN JVP IN A CASE OF HOCM ? WHY ?
    • Prominent ‘ a ’ waves are seen
    • It indicates hypertrophy of ventricular septum leading to lack of compliance of right ventricle
  • CVS EXAMINATION
    • INSPECTION
      • Apex visible in 6 th intercostal space 1cm outside MCL
      • Diffuse apical impulse
      • No precordial bulge
    • PALPATION
      • Double apical impulse felt
      • S4+
      • No thrill
      • No PSH
  • WHAT ARE THE CAUSES OF DOUBLE AND TRIPLE APICAL IMPULSE ?
    • Double apical impulse
    • Decreased LV compliance
    • Pre-systolic apical impulse due to forceful atrial systole
    • Triple apical impulse
    • Late systolic bulge of left ventricle that occurs when heart is almost empty and is in near iso-metric contraction
    • AUSCULTATION
    • S1 normal
    • S2 split – paradoxical
    • Harsh cresendo-decresendo mid-systolic murmur grade III/VI heard between apex and left sternal border not radiating to carotid or axilla
    • Murmur increases with standing, exercise, Valsalva maneuver (strain)
    • Decreases with squatting, isometric hand grip, Valsalva maneuver (overshoot)
  • WHAT ARE THE CAUSES OF PARADOXICAL SPLIT S2 ?
  • LBBB RV PACING RV ECTOPY DELAYED ELECTRICAL ACTIVATION OF LV EARLY ELECTRICAL ACTIVATION OF RV AS IN TYPE B WPW SYNDROME. IN WPW SYNDROME, REVERSED SPLIT OCCURS ONLY WHEN THERE IS SIGNIFICANT PRE-EXCITATION SEVERE TRICUSPID REGURGITATION EARLY PULMONIC CLOSURE ANEURYSM OF ASCENDING AORTA POST-STENOTIC DILATION IN AS INCREASE OF HANGOUT INTERVAL ON THE AORTIC SIDE SEVERE AS SEVERE SYSTEMIC HYPERTENSION ACUTE MYOCARDIAL INFARCTION DURING AN EPISODE OF ANGINA CARDIOMYOPATHY SEVERE AR LARGE PATENT DUCTUS ARTERIOSIS PROLONGED LV MECHANICAL SYSTOLE CAUSES MECHANISM
  • WHAT TYPE OF MURMURS CAN BE HEARD IN HOCM ?
    • Harsh cresendo-decrescendo systolic murmur
    • Holosystolic murmur of mitral regurgitation
    • Diastolic rumbling murmur in patients with severe MR
    • Murmur of aortic regurgitation
    • OTHER SYSTEM EXAMINATION : NAD
  • INVESTIGATION WNL LIVER PROFILE WNL RENAL PROFILE WNL HEMOGRAM
  • INVESTIGATION NORMAL SINUS RHYTHM AXIS : (– 30°) LEFT ATRIAL ENLARGEMENT POOR PROGRESSION OF R WAVE LVH PRESENT LARGE NEGATIVE PRECORDIAL T WAVES ECG
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  • WHAT ARE THE ECG CHANGES FOUND IN HOCM ?
    • ST-T wave abnormalities
    • QRS complexes, tallest in the midprecordial leads
    • Prominent Q waves in precordial leads
    • Giant negative T waves
    • Evidence of LAE/RAE
    • Short PR interval
    • Prolongation of QTc
    • Features of WPW syndrome
    • Arrhythmias- VPCs, VT, SVT, AF
  • DIMENSIONS LA – 40mm IVS(D) – 27mm LVPW(D) – 10mm IVS(S) - 30mm LVPW(S) – 19mm LVEF – 77% ASH + GROUND GLASS APPEARANCE OF SEPTUM LVOT Δ RESTING 27 mmHg POST-SORBITRATE 60 mmHg ECHO
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  • OCCASIONAL SVCS VPCS OF RBBB, LBBB MORPHOLOGY ONE COUPLET ONE RUN OF 3 BEATS NO SINUS PAUSE ASYMPTOMATIC DURING RECORD HOLTER
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  • WHO ARE THE PATIENTS AT HIGH RISK FOR SCD ?
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  • COURSE OF EVENTS
  • FINAL DIAGNOSIS
    • A CASE OF HYPERTROPHIC OBSTRUCTIVE CARDIOMYOPATHY, NYHA CLASS III, IN NORMAL SINUS RHYTHM, WITH NO EVIDENCE OF INFECTIVE ENDOCARDITIS WITH HIGH RISK FOR SCD
  • MANAGEMENT PLAN
    • PRIORITIES OF THERAPY
    • Alleviation of symptoms
    • Prevention of complications
    • Prevention of sudden cardiac death
    • Management of heart failure
  • TREATMENT
    • PHARMACOLOGICAL
    • Atenolol 100mg 1OD
    • Verapamil 40mg 1TDS
    • NON-PHARMACOLOGICAL
    • Alcohol septal ablation
  • IMPORTANT POINTS TO REMEMBER ABOUT HOCM
    • First described by Sir Russell Brock in 1958
    • Eugene Braunwald described the unique hemodynamics
    • Other terms used are idiopathic hypertrophic subaortic stenosis and muscular subaortic stenosis
    • Defined as myocardial hypertrophy in absence of identifiable cause
    • Prevalence is 1:500 to 1:1000
    • Autosomal dominant disease
    • Most common genetically transmitted cardiovascular disease
    • Genetic basis first reported by Seidman and Seidman (chromosome 14q11-12)
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    • Most common cause of SCD in young including trained athletes
    • Common sites of ventricular involvement are septum, apex and mid-ventricle in decreasing order of frequency
    • Obstruction present in 25% of cases
    • Most characteristic is diastolic dysfunction rather than systolic
    • Triad of dyspnea, angina, syncope
    • Most common symptom is dyspnea
    • Angina in 70-80% cases
    • MI in 15% cases
    • Syncope in 20%, over 50% have pre-syncope
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    • B-blocker is the initial drug of choice
    • Advantages – decreased heart rate response to exercise
    • Decreased outflow gradient with exercise
    • Decreased oxygen demand
    • Improvement in diastolic filling
    • Ca-channel blockers improves abnormal diastolic relaxation
    • Disopyramide with negative inotropic effect decreases the gradient and improve symptoms
    • Disopyramide added to B-blocker or Ca-blocker if symptoms persist
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    • Pacing of right ventricular apex reduces SAM
    • Pacing or sensing atrium helps to maintain hemodynamic contribution of atrial contraction
    • Used in patients with assd. sinus or AV node dysfunction
    • Used in elderly patient with multiple co-morbidities who are at high risk for other therapeutic modalities
    • Alcohol septal ablation is new therapeutic modality
    • 100% alcohol is infused in first septal perforator artey
    • Produces controlled MI of proximal septum
    • Remodelling of basal septum region results in reduction of outflow obstruction
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  • THANK YOU