Year : 2021 Month : April Volume : 10 Issue : 14 Page : 1035-1038

Severe Vascular Complications Following Thrombolytic Therapy in a Case of Prosthetic Mitral Valve Thrombosis – A Case Report

Ayan Husain1, Shilpa Abhay Gaidhane2, Priti Abhay Karadbhajane3, Sourya Acharya4, Apoorva Nirmal5

1, 2, 3, 4, 5 Department of Medicine, Jawaharlal Nehru Medical College, DMIMS
(Deemed to Be University), Sawangi (Meghe), Wardha, Maharashtra, India.


Dr. Shilpa Gaidhane, Department of Medicine, Jawaharlal Nehru Medical College, DMIMS (Deemed to Be University), Sawangi (Meghe), Wardha, Maharashtra, India.
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Prosthetic cardiac valve thrombosis is a rare but dangerous complication;1,2 particularly in patients with low conformity on anticoagulant therapy. Thromboembolic problems happen after mechanical valve substitution in 0.5 - 8 percent.3-5 Fibrinolytic therapy to treat the thrombosis is widely used nowadays with high efficacy and no severe side effects as compared to emergency surgical treatment, which is associated with high mortality.6

Surgical valve repair in patients with rheumatic heart disease remains the gold standard for the treatment. Thrombosis of the prosthetic heart valve in patients undergoing valve replacement, is the most severe and deadly complication. Currently, the treatments available for symptomatic prosthetic valve thrombosis are immediate surgery or thrombolytic therapy (TT). In rural hospital settings patients are poor and there is a lack of surgical expertise. These factors make TT the perfect treatment for prosthetic valve thrombosis. But one should be aware of embolic complications.


A 30-year-old male patient a known case of rheumatic heart disease with severe mitral stenosis underwent mitral valve replacement with TTK Chitra mitral prosthesis in 2017. Two years later, he presented to the Emergency Department of Medicine at night 8 pm with complaints of, sudden onset of breathlessness, chest pain and orthopnoea for 24 hours. He had stopped taking anticoagulants a month back due to financial constraints.

On examination, heart rate - 115 / min, BP - 86 / 50 mmHg, jugular venous pressure (JVP) raised. Metallic click could not be heard, bilateral crepitations present. Electrocardiogram-atrial fibrillation (ECG–AF) with FVR with right ventricular hypertrophy. Haemoglobin (Hb) - 14.6 g / dl, white blood cell (WBC) - 13900 / mm,3 platelets - 1.56 lac / mm,3 creatinine - 1.1, liver function test (LFT) normal and international normalised ratio (INR) 1.08. Blood cultures showed no growth of any organisms. Clinical diagnosis of a thrombotic mitral valve thrombosis was confirmed by transthoracic echocardiography. The effective valve area was 0.45 cm2 with evidence of 1cm2 thrombus and an increased mean peak gradient (23 mmHg) across the mitral valve (Figure 1).







Therefore, dobutamine along with furosemide were infused continuously for cardiogenic shock and acute pulmonary oedema, and intravenous diltiazem was given for heart rate control. Fibrinolytic therapy with streptokinase was given because of the unavailability of vascular surgeon at the time of presentation. Within 3 hours after the start of therapy the patient's symptoms of heart failure had improved markedly but he developed pain and weakness of both lower limbs, more in left side as compared to right side. Peripheral pulsations could not be palpated in both the lower limbs below the femoral artery. 2D-ECHO post thrombolysis-good leaflet motion of mitral valve and peak gradient of 8 mmHg across the valve with no thrombus or vegetation. The calculated mitral valve area increased to 1.65 cm.2 Bilateral lower limb angiography was done immediately which showed saddle thrombus at aortic bifurcation. (Figure 2) with slow reformation of bilateral iliac arteries. Thrombectomy was done by the vascular surgeon at our institute and parenteral anticoagulants were started.

After three days, right lower limb symptoms resolved. But only partial relief of symptoms in left lower limb and there was left sided foot drop after 5 - 6 days, the patient started developing blackening of left lower limbs digits without any clear-cut line of demarcation. (Figure 3). Check angiography revealed no saddle thrombus at aortic bifurcation, good distal flow in right common iliac artery and below (Figure 4) but there was long segment subacute thrombus in left distal superficial femoral artery (Figure 5). There was no gangrene and the pain decreased. Patient was managed conservatively, and he was discharged on oral anticoagulants, antiplatelets and analgesics. Followed up with us one month later. The blackening of digits had recovered. Doppler showed partial thrombotic narrowing of superficial femoral artery with good collateral circulation.



Prosthetic valve thrombosis (PVT) is a very serious complication after valve replacement. Factors predisposing to thrombosis include atrial fibrillation, sub-therapeutic anticoagulation and irregular INR monitoring, and pregnancy. Mitral valve is approximately twice as commonly involved as aortic valve.1,2 The most common complications of PVT are valvular obstruction or stenosis and thromboembolism. The reported incidence of symptomatic obstructive mechanical PVT ranges from 0.2 to 8 % per year in India and it is more common (6 %) in patients receiving sub-therapeutic anticoagulation.3-5 The rate of thromboembolism after PVT during the first 6 months is significantly more and it is highest during the first 30 days.6-8 The risk of thromboembolism is least in patients with bio-prosthetic valves (who are generally not anti-coagulated), higher with patients of mechanical valves who are anticoagulated and highest in patients of mechanical valves receiving inadequate anti-coagulation.9 High mortality and morbidity are associated with prosthetic valve thrombosis.10

Prosthetic valve thrombosis has been split into two forms: obstructive (embolus of more than 10 mm2) and non-obstructive (embolus of less than 10 mm2) prosthetic valve thrombosis and their therapeutic approach.10

Valvular obstruction may present with heart failure, presyncope or syncope and in rare cases sudden cardiac death. Left sided PVT may cause systemic embolic complications such as stroke, peripheral gangrene or less frequently myocardial infarction. Right sided PVT can complicate into pulmonary embolism and rarely systemic embolic events via paradoxical embolism.11

The diagnostic criteria on echo cardiac for PVT are decreased valve strength, mass over the valve (thrombus), decreased effective prosthetic area, and trans prosthetic valve flow, prosthetic valve incompetence, increased trans-prosthetic gradients.12 Treatment modality depends on i) existence of distortion of the valve, ii) Medical status of the patient, iii) the thrombus size, iv) The local level of medicine and economy, and v) the experience with reoperation. Hospitals that do not have practice with reoperation or location of financially poor regions have a high surgical cost, making TT the perfect treatment for PVT.13

Mechanical PVT is managed mainly by fibrinolysis or by surgery (thrombectomy and valve replacement) along with supportive treatment of heart failure and anticoagulation with unfractionated heparin (Table 1).1 In our case thrombolysis was preferred due to high New York Heart Association (NYHA) Class, and un-availability of surgeon and expertise with re