A Case Of Valvular Heart Disease With Stroke Biology Essay


This 30 year old lady was a known case of RHD with severe MS, MR and TR with pulmonary artery hypertension in sinus rhythm. She presented with acute onset right sided hemiparesis with facial involvement with aphasia due to a left MCA infarct. She was thrombolysed with tissue plasminogen activator with good neurological recovery. Within a few days she was taken up for mitral valve replacement. An approach to such a case is discussed.

Clinical summary

This 30 year old right handed housewife presented with history of breathlessness of last 11 years and palpitations for the last 5 years. She was in NYHA class III with no h/o orthopnoea or PND. On examination her BMI was 15.4 kg/m2 and pulse was 84/min, regularly regular. Cardiovascular examination revealed a precordial bulge, apex beat in the5th ICS one cm lateral to the left mid clavicular line, tapping in character. There was a Grade 1 left para sternal heave (LPSH) present. A diastolic thrill was present over mitral area and the second heart sound was palpable. On auscultation, first heart sound was soft; P2 component of second heart sound was loud. An opening snap was heard. A low pitched rumbling mid diastolic murmur with pre systolic accentuation was heard best over the apex with bell of stethoscope in left lateral position in expiration. A blowing Gd III/VI pansystolic murmur was heard at the apex with radiation to the axilla. There was another pan systolic murmur heard at the tricuspid area which increased in intensity on inspiration and leg raising.

What is the diagnosis?

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A case of valvular heart disease, likely rheumatic in etiology with severe mitral stenosis (MS), moderate mitral regurgitation (MR) and tricuspid regurgitation (TR) with pulmonary artery hypertension in normal sinus rhythm, no feature of congestive cardiac failure in NYHA Class III with no evidence of fresh rheumatic activity or infective endocarditis.

At the bedside how does one assess the severity of MS?

On auscultation of a patient with severe MS narrow A2-OS gap and longer duration of mid diastolic murmur would suggest severe MS. Other indirect evidence includes symptomatic patient and clinical evidence of right ventricular hypertrophy with pulmonary hypertension.

What clinical signs does this patient have of pulmonary hypertension?

Loud and palpable S2, LPSH and murmur of TR.

What is the bedside evidence of infective endocarditis?

Fever, anemia, clubbing, Osler's Nodes (Fig 1), splinter hemorrhage, Janeway's lesion (Fig 2), petechiae, change in the character of a pre existing murmur or appearance of a new murmur, splenomegaly and Roth's spots (Fig 3) are the bed side signs which suggest infective endocarditis.

Figure1: Osler's node in the pulp of the finger

Figure 2: Janeway lesion in the palm of the hand

Figure 3: Roth's spot seen on fundus examination


Haemogram and chemistries were normal, ECG was normal. X-ray chest (Fig 5) showed straightening of left heart border, cardiomegaly, upper lobe venous diversions, prominent pulmonary arteries and double atrial density. Echocardiography showed an increased left atrial size of 60 mm, EF -65%. The mitral valve was thickened, calcific and doming with a mitral valve area of 0.8 cm2 suggestive of severe MS. There was moderate MR and TR. Aortic valve was normal. A left atrial thrombus was present.

Figure 4: X-ray chest showing straightening of the left heart border, cardiomegaly, prominent pulmonary artery and double density atrial shadow

What are the intervention options available for a patient with MS?

Percutaneous Balloon Mitral Valvotomy (PBMV), surgical (open) valvotomy and mitral valve repair, and Mitral Valve Replacement (MVR).

What are the prerequisites for PBMV?

Symptomatic patient (NYHA Class II or more)

MVA < 1.5 cm2

Relatively pliable valve leaflet

Little or no commisural calcium

Sub valvular apparatus is relatively free of scarring and thickeness

No LA clot

What would be the intervention option in this patient other than medical management and why?

This patient will need mitral valve replacement (MVR) because of the presence of significant MR in addition to severe MS. In addition she also has a LA clot and thickened calcific valve.


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She was started on medical management with Inj benzathine penicllin 1.2 MU every 3 weekly, atenolol 25 mg OD and a diuretic. She was admitted for work up for mitral valve surgery.While being admitted to the ward she developed acute onset right sided hemiparesis with facial involvement and inability to speak. On examination the pulse was regular. Neurological examination revealed conscious patient with motor aphasia, right upper motor neuron seventh nerve palsy with right sided hemiplegia (power 0/5). National Institute of Health Stroke Scale (NIHSS) score was 16. NCCT brain was normal.

Patient was thrombolysed with Alteplase 0.9 mg /kg, 4 mg of iv bolus followed by 32 mg infusion over 1 h and 24 hours after thrombolysis anticoagulation was started. She responded to thrombolytic therapy in the form that at 6 hours after the thrombolysis the motor aphasia improved and NIHSS was 12; 24 hours later she was ambulant with minimal support and the NIHSS was 06 and at 48 hours she was ambulant without support and performing all activities of daily living

What is the likely event that has occurred and why?

The patient appears to have developed a cardio embolic stroke in the left middle cerebral artery.

What are the early signs of stroke on CT?

Figure 5: loss of insular ribbon Figure 6: Obsucration of lentiform nucleus

Fig 7: Loss of grey and white matter differentiation Fig 8: Hyperdense MCA sign

Other signs include subtle effacement of cortical sulci and local mass effect. Early signs of ischaemia on CT have ranged in different studies from 31% in < 3h (Patel SC, JAMA 2001) to 81% < 5h of MCA stroke (Von Kummer, AJNR, 1994)

What is the window period for thrombolysis in acute ischemic stroke as per present guidelines?

4.5 hours.

What are the contraindications to thrombolysis?


Stroke or head trauma in the previous 3 months

Any history of intracranial haemorrhage

Major surgery in the previous 14 days

Gastrointestinal or urinary tract bleeding in the previous 21 days

Myocardial infarction in the previous 3 months

Arterial puncture at a noncompressible site in the previous 7 days


Spontaneously clearing stroke symptoms

Only minor and isolated neurologic signs

Seizure at the onset

Symptoms of stroke suggestive of subarachnoid haemorrhage

Persistent blood pressure elevation (systolic ≥185 mmHg, diastolic ≥110 mmHg)

Active bleeding or acute trauma (fracture) on examination

For treatment from 3 to 4.5 hours, an additional relative exclusion (where the risk/benefit ratio is less clear) is an NIH Stroke Scale score of >25


Platelets <100,000/mm3

Serum glucose <50 mg/dl (<2.8 mmol/L)

International normalized ratio (INR) >1.7 if on oral anticoagulant

Elevated partial thromboplastin time (aPTT) if on heparin

Head CT scan

Evidence of haemorrhage

Evidence of a multilobar infarction with hypodensity involving >33 percent of the cerebral hemisphere

What is the most significant complication of thrombolysis?

The most significant complication of thrombolysis is intracerebral hemorrhage (ICH). Symptomatic ICH may occur in 3-7% of patients.

At the bedside when should ICH during or post thrombolysis is suspected?

One should suspect ICH if within 24 hours of thrombolysis there is:

Appearance of headache


Worsening of sensorium

Worsening of deficit or appearance of new deficit

Sudden rise in BP

What action should a resident take if symptomatic ICH is suspected?

AHA/ASA Recommendation 2007 for post thrombolysis symptomatic ICH are:

Stop thrombolysis

Arrange for an immediate CT

Samples to be drawn for typing and cross matching, prothrombin time, activated partial thromboplastin time, platelet count, and fibrinogen.

If intracerebral haemorrhage is confirmed by imaging with significant mass effect:

Give 10 units of cryoprecipitate to increase the levels of fibrinogen and factor VIII

Give 6 to 8 units of platelets

Role of neurosurgical evacuation is controversial

The patient recovered well and 10 day post stroke MRI showed a small infarct (Fig 9). Within two weeks of the stroke she underwent mitral valve replacement (MVR) with #27mm ON-X valve (Fig 10). During the surgery the left atrial appendage was removed along with the LA clot. Intra-operatively she was found to have cardiomegaly, enlarged right atrium, thickened mitral valve and highly deformed severe subvalvular pathology. Post operative recovery was uneventful. Patient was discharged on anticoagulant and diuretic with advice to maintain an INR around 2.5 - 3.5.

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Figure 9: MRI brain showing axial FLAIR images of a infarct in left internal capsule

Figure 10: ON-X valve

As an internist following up this case with mechanical prosthetic heart valve what are the complications one can expect?

Paravalvular leaks

Valve obstruction due to thrombosis

Systemic embolization


Endocarditis and other infections

Hemolytic anemia

Final Diagnosis

RHD with severe MS, MR (MVR done) and TR with pulmonary hypertension, in sinus rhythm, not in congestive cardiac failure, no evidence of fresh rheumatic activity or infective endocarditis in NYHA class III.

Right hemiparesis with upper motor neuron facial weakness with Broca's aphasia due to left MCA stroke, thrombolysed with complete functional recovery.


Cardioembolic strokes commonly occur in patients with rheumatic heart disease. The risk increases if the patient has atrial fibrillation or paroxysmal atrial fibrillation, mitral or aortic valve disease and the presence of left atrial thrombus. In addition to the other risk factors mentioned this patient had possibly transient atrial fibrillation.

Cardioembolic strokes can also be thrombolysed safely. They need to be started on anticoagulation in adequate doses after thrombolysis to prevent recurrence. Although the window for thrombolysis is extended to 4.5 hours the best results are obtained if thrombolysis is started as early as possible. Hence a door to needle time of around 30-45 minutes should be attempted in all centres. To minimize the chances of symptomatic intra cerebral hemorrhage a checklist of contraindications for thrombolysis must be excluded.

Surgery for removal of left atrial thrombus and subsequent valve replacement should not be postponed even after a recent stroke since that will prevent a recurrence.

Take Home Message

Thrombolysis for ischemic stroke in selected cases can be safe and result in excellent neurological recovery if administered on time.

A recent stroke is not a contraindication for cardiac surgery for left atrial thrombus because that subgroup of patients is likely to benefit the most.

Suggested Reading

SmithWS, English JD, Johnston SC. Cerebrovascular Diseases In: Fauci, Braunwald, Kasper Ed. Harisson's Principles of Internal Medicine 17 th edition. McGraw Hill 2008: 2513-2535.

Biller Jose, Love BB, Schneck MJ. Ischemic Cerebrovascular Disease In: Bradley WG, Daroff RB Ed. Neurology in Clinical Practice 5th edition. Butterworth Heinemann Elsevier 2008: 1165-1224.