DEPARTMENT OF INTERNAL MEDICINE II AND PHTHYSIATRY

-RAJKUMAR SUBASARAVANAN
SUBGROUP ”12”
CARDIOMYOPATHY:
 The cardiomyopathies are a group of diseases that primarily affect the heart muscle and are not the result of
congenital, acquired valvular, hypertensive, coronary arterial, or pericardial abnormalities.
 Two fundamental forms of cardiomyopathy are recognized:
1) Primary type, consisting of heart muscle dis- ease predominantly involving the myocardium and/or of
unknown cause;
2) Secondary type, consisting of myocardial disease of known cause or associated with a systemic disease such
as amyloidosis or chronic alcohol use .
CLASSIFICATION:
ACC/AHA CLASSIFICATION:
ETIOLOGY:
PATHOGENESIS AND CLINICAL FINDINGS:
CLINICS:
DIAGNOSTICS:
HYPERTROPHIC CARDIOMYOPATHY:
CHEST X-RAY:

Marked Cardiac Silhouette enlargement

ECHO FINDINGS:
ECG FINDINGS:
 Left anterior hemiblock
 Left ventricular hypertrophy
 Deep T wave inversion
 Prolonged QT interval.
• Left Ventricular Hypertrophy results in increased precordial voltages and non-specific ST segment and T-wave
abnormalities.
• Asymmetrical septal hypertrophy produces deep, narrow (“dagger-like”) Q waves in the lateral (V5-6, I, aVL)
and inferior (II, III, aVF) leads. These may mimic prior myocardial infarction, although the Q-wave morphology
is different: infarction Q waves are typically > 40 ms duration while septal Q waves in HCM are < 40 ms. Lateral
Q waves are more common than inferior Q waves in HCM.
• Left ventricular diastolic dysfunction may lead to compensatory left atrial hypertrophy, with signs of left
atrial enlargement (“P mitrale“) on the ECG.
• There is an association between HCM and Wolff-Parkinson-White (WPW) syndrome: ECG features of WPW
were seen in 33% of patients with HCM in one study. At least one genetic mutation has been identified that
is associated with both conditions.
• Atrial Fibrillation and Supraventricular Tachycardias are common
ASYMMETRIC SEPTAL HYPERTROPHIC CARDIOMYOPATHY:

Voltage criteria for left ventricular hypertrophy.

Deep narrow Q waves < 40 ms wide in the lateral leads I, aVL and V5-6.
APICAL HYPERTROPHIC CARDIOMYOPATHY:

Large precordial voltages.

Giant T wave inversions in the precordial leads
Inverted T waves are also seen in the inferior and lateral leads.
DILATED CARDIOMYOPATHY:
CHEST X-RAY:

Mild cardiac silhouette enlargement

ECHO FINDINGS:
ECG FINDINGS:

 Sinus tachycardia
 Bundle branch block
 Left anterior hemiblock
 Reduced QRS complexes
 Ventricular tachyarrhythmias
 There is marked  Left Ventricular Hypertrophy  with repolarisation abnormality (LV “strain” pattern) in V5-6.
 LV dilatation has produced an interventricular conduction delay mimicking LBBB — however, this is not LBBB
as the morphology is not typical and there are small Q waves in V5-6 (the presence of Q waves in V6 rules out
LBBB).
 There are some signs of left atrial enlargement — leftward deviation of the P wave axis (positive P waves in I
and aVL, inverted in III and aVF) and prolongation of the terminal portion of the P wave in V1.
 Right axis deviation in the presence of LVH suggests the possibility of biventricular enlargement.
 The widespread downsloping ST depression may be due to LVH 
RESTRICTED CARDIOMYOPATHY:
CHEST X-RAY:

Marked cardiac silhouette enlargement

ECHO FINDINGS:
CARDIAC MAGNETIC RESONANCE IMAGING(CMRI):

Cardiac magnetic resonance imaging of patient with cardiac amyloidosis.

 A, Early gadolinium phase. Note the thickened heart walls.
 B, Diffuse late gadolinium enhancement of the myocardium.
ECG FINDINGS:
 Low voltage QRS Complexes
 Non-specific ST segment / T wave changes
 Bundle branch blocks
 Atrioventricular block (3rd degree AV block may
occur in sarcoidosis)
 Pathological Q waves
 Atrial and ventricular dysrhythmias
 Low voltage QRS complexes
Non specific ST segment/ T wave changes
TREATMENT ALGORITHMS: HYPERTROPHIC CARDIOMYOPATHY
DILATED CARDIOMYOPATHY:
RESTRICTIVE CARDIOMYOPATHY:
No specific treatment. Only treatment of underlying conditions.
INDICATIONS FOR PACEMAKER IMPLANTATION:
o Patients with idiopathic restrictive cardiomyopathy (RCM).
o Patients with amyloidosis, If cardioversion to treat atrial fibrillation is attempted.
o Patients with sinus node dysfunction and/or advanced conduction system disease.
TRANSIENT FORM OF CARDIOMYOPATHY:
TYPES:
ECHO AND CORONAROGRAM FINDINGS:

A,B-Transient akinesis / dyskinesis of left

ventricle (apical and mid-ventricular
segments) with regional wall abnormalities
extending beyond a single vascular territory.
C,D-Absence of coronary artery stenosis
>50% or culprit lesion
ECG FINDINGS:

New ECG changes (ST elevation or T wave inversion) or moderate troponin rise(Labs).
MANAGEMENT AND TREATMENT:
• Managed by supportive therapy resulting in rapid symptom
resolution.
• Stress management by meditation and by other means.
• Psychotherapy.
CASE 1:
• A 58 year-old-woman with no medical history, presented to the emergency department complaining of
oppressive chest pain of moderate intensity accompanied by dyspnea 6-h lasting.
• An electrocardiogram (ECG) was performed on admission, which showed ST-segment elevation in
precordial leads from V1 to V5, and T-wave inversion from V4 to V6 .Initial troponin I determination
showed a value of 3.7ng/ml which was above the 99th percentile upper reference limit.
• The following troponin serum levels were 2.9ng/ml and 1.3ng/ml, which were lower than those expected
for the magnitude of ST segment elevation.
• ECG:
A) ECG recording at presentation showed ST-segment elevation in precordial leads from V1 to V5 and T-
wave inversion in V4–V6.
B) ECG recording at the third day of hospitalization showing progression from ST segment elevation to
inverted symmetrical T-waves in all precordial leads.
• CORONAROGRAM:
(A) Right coronary artery in RAO view without evidence of obstructive lesions.

(B) left coronary artery in RAO view without evidence of obstructive lesion in any segment.
 VENTRICULOGRAPHY in RAO view showing motion abnormalities of the left ventricle.
(A) end-diastole, (B) end-systole, (C) the same image seen in A but with enhanced endocardial border which shows normal
cavity contours, and (D) the same image seen in B but with enhanced endocardial borders showing a pattern of apical
ballooning, impaired mid-ventricular contractility and normal motion of the basal segments.
CASE 2:
• A 66-year-old independently functioning woman presented to the emergency room with an episode of mid-
epigastric and left sternal chest pain.
• Her medical history included hypertension, hyperlipidemia, glaucoma, and multiple previous episodes of
chest pain similar to her current episode that necessitated three separate coronary angiograms which
showed no stenotic or occluding lesions in the coronary arteries.
• The patient described her chest pain as a sensation of burning that started suddenly at 11 pm in the night
while she was resting comfortably at home after having dinner. The pain was mild in intensity, nonradiating,
and lasted for a few minutes before resolving spontaneously. She denied having any dyspnea, palpitations,
dizziness, or loss of consciousness during this episode.
• She had no history of smoking or illicit drug use.
• Her vital signs were as follows: blood pressure of 168/46 mmHg (right arm, supine position), heart rate of
66/min, respiratory rate of 19/min, and an oral temperature of 97.9 F.
• An electrocardiogram was obtained which showed a normal sinus cardiac rhythm with a left bundle branch
block, possible left ventricular hypertrophy, and T wave inversions in the lateral leads. No ST segment
changes were noted .
• Her laboratory data included a cardiac troponin level of 0.15 ng/ml. Follow-up cardiac troponin levels
obtained 6 and 12 hours later were 4 ng/ml and 9 ng/ml, respectively.
EKG showing normal sinus cardiac rhythm with a left bundle branch block, possible
left ventricular hypertrophy, and T wave inversions in the lateral leads.
No ST segment changes were noted.
Coronary angiogram showing normal left main, left anterior descending, left
circumflex, and right coronary arteries with no stenotic or occluding lesions.
Cardiac left ventriculogram done by cardiac chamber catheterization
confirming the echocardiographic finding of apical hypertrophy.
REFERENCES:
1. Harrison’s principles of internal medicine. Seventeenth Edition / Anthony S. Fauci,
Dennis L. Kasper, Dan L. Longo [et al.] // New York. – McGraw-Hill, Medical Pub.
Division. – 2008. – 3778 P.
2. Reardon L. Restrictive Cardiomyopathy [Electronic resource] / Lindsay Reardon. –
2017. – Re- source access mode: https://emedicine.medscape.com/article/153062-
overview.
3. Nguyen V.Q. Dilated Cardiomyopathy [Electronic resource] / Vinh Q Nguyen. – 2017.
– Re- source access mode: https://emedicine.medscape.com/article/152696-
overview
4. Shah N.S. Hypertrophic Cardiomyopathy [Electronic resource] / Sandy N Shah. –
2016. – Re- source access mode: https://emedicine.medscape.com/article/152913-
overview
5. What is Cardiac Rehabilitation? [Electronic resource] – Resource access mode:
http://www. heart.org/HEARTORG/Conditions/More/CardiacRehab/What-is-Cardiac-
Rehabilitation_ UCM_307049_Article.jsp#.WrApyea-k8o.
6. Tang W.H.W. Myocarditis [Electronic resource] / Wai Hong Wilson Tang. – 2016. –
Resource access mode: https://emedicine.medscape.com/article/156330-overview