Lupine publishers|Study Of Clinical Characteristics and Risk Determinants Of Patients With Prosthetic Valve Thrombosis: A Tertiary Care Hospital-Based Observational Study
Lupine publishers|Advancements in Cardiology Research & Reports
Prosthetic valve replacement is the mainstay of treatment for patients with severe symptomatic valvular heart disease but in the process, the native valvular disease is exchanged with prosthesis-related complications. The prosthetic valve dysfunction due to the formation of thrombus, pannus formation, infective endocarditis or paravalvular leak [1]. Prosthetic valve thrombosis (PVT) is a rare but serious complication of valve replacement, most often encountered with mechanical prostheses. PVT has been further divided into Obstructive and Non-Obstructive PVT. The incidence of obstructive PVT for mechanical valves varies between 0.3-1.3-3% patient years[2,3]. The incidence ranges from 0.1% to almost 6% per patient-year for left-sided valves and up to 20% for tricuspid valves[4] .The etiology of PVT is complex and multifactorial. The Sub-optimum anticoagulation is the major cause of prosthetic valve thrombosis in addition to type and position of the prosthetic valve, presence or absence of pro-thrombotic states like atrial fibrillation, and ventricular dysfunction[5,6].PVT may present with progressive dyspnea, signs of heart failure, or systemic embolization, or may be incidentally diagnosed during the routine echocardiographic follow-up. Various modalities aid in the diagnosis of PVT. Trans-thoracic echo (TTE) is the initial screening tool. Trans-esophageal echo (TEE) and Cine-fluoroscopic leaflet mobility profile are further done to establish the pathology[4][6-8]. Various Treatment modalities for treat prosthetic valve dysfunction include intensification of anticoagulation, thrombolytic therapy, surgical thrombectomy, and prosthetic valve replacement. However one should try to prevent this dreadful complication by meticulous monitoring of patient profile and symptomatology at every clinical visit. We conducted a prospective observational study of all patients presenting with PVT. Patients with prosthetic valve thrombosis were diagnosed based on standard criteria and clinical characteristics, risk determinants, treatments, and outcomes were assessed. Material and MethodsThis was a prospective observational study conducted in a tertiary care institute, The study was duly approved by the institutional review board and ethical committee.Inclusion Criteria All consecutive eligible participants consenting to participate suspected of having prosthetic valve dysfunction based on clinical, echocardiographic, and fluoroscopic findings would be screened for enrollment in the study.Exclusion CriteriaPatient not consenting to participate in the study.Definition Of PvtIt was defined on 3 criteria; Clinical, Echocardiographic and Fluoroscopic. A.Clinical Criteria:1)Shortness of breath 2)Features of systemic embolization.B.Echo Criteria1)Increased gradients when compared with the reference values. 2)Prosthetic valve thrombus was recognized as soft and homogeneous, mobile or fixed echo densities located at the valve occluder and/or valve struts. The largest diameter of the thrombus as well as the length of the mobile portion, if present was measured.3)A diagnosis of pannus formation was made when fixed, bright echo dense structures, sometimes containing focal calcific deposits, were present primarily along the valve ring with extension into the valve oriC.Fluoroscopic CriteriaEach prosthesis was viewed in multiple projections including caudocranial angulations, which allowed proper visualization of prosthesis leaflet motion; that opening and closing angles were calculated. A short cine fluoroscopic film( usually 3 to 10 cardiac cycles) at 50 frames/s was recorded.Response to TreatmentComplete Response - Complete success was defined as normal or near-normal transvalvular gradient and restoration of normal leaflet motion on fluoroscopy without any major complications and clinical improvement in symptomsPartial Response -
Partial success was defined as a reduction of > 50% of transvalvular gradient from the baseline or complete hemodynamic response with major complication or restricted movement of prosthetic valve leaflets on cine fluoroscopy even though the transvalvular gradients completely normalized. Failed Treatment - Failure of TT was defined as no hemodynamic response even with extended thrombolysis (up to 72 h) or death by major complications.Predefined Complications :•All-cause in-hospital mortality.•Non- fatal minor complications-bleeding without need for transfusion; TIA.•Non-fatal major complications-ischemic stroke, ICH, embolism(coronary or peripheral), bleeding requiring transfusion.Various Treatment Regimes for Thrombolytic Agents:1.Streptokinase regimen- 2.5 lakh IU intravenous bolus for 30 minutes followed by slow intravenous infusion at the rate of 1 lakh IU/hr2.Tenecteplase -slow intravenous infusion for 0.5mg/kg as an intravenous infusion for up to 72 hours in failed cases.3.Alteplase- slow intravenous infusion of 0.5mg/kg/hr.Response to Treatment :1.Serial echocardiography - Bedside echocardiography was done every six hours and gradients and valve area was recorded2.Serial fluoroscopy was done every 12 hours and opening and closing angles were determined.Once the complete response was achieved, infusion of thrombolytic agents was stopped or was continued till 72 hours in cases of failed or partial response. Premature cessation of Citation:Vaishali Verma, Sanjeev Asotra*, Rajesh Sharma, PC Negi, Arvind Kandoria, Neeraj Ganju, Rajeev Marwaha, Shivani Rao, Kunal Mahajan and Ashu Gupta. Study Of Clinical Characteristics and Risk Determinants Of Patients With Prosthetic Valve Thrombosis: A Tertiary Care Hospital-Based Observational Study. Adv Card Res 3(4)- 2021. ACRR.MS.ID.000170. DOI: 10.32474/ACR.2021.03.000170Volume 3 - Issue 4Adv Card Res.Copyrights @Sanjeev Asotra, et al.352The etiology of PVT is complex and multifactorial. The Sub-optimum anticoagulation is the major cause of prosthetic valve thrombosis in addition to type and position of the prosthetic valve, presence or absence of pro-thrombotic states like atrial fibrillation, and ventricular dysfunction[5,6].PVT may present with progressive dyspnea, signs of heart failure, or systemic embolization, or may be incidentally diagnosed during the routine echocardiographic follow-up. Various modalities aid in the diagnosis of PVT. Trans-thoracic echo (TTE) is the initial screening tool. Trans-esophageal echo (TEE) and Cine-fluoroscopic leaflet mobility profile are further done to establish the pathology[4][6-8]. Various Treatment modalities for treat prosthetic valve dysfunction include intensification of anticoagulation, thrombolytic therapy, surgical thrombectomy, and prosthetic valve replacement. However one should try to prevent this dreadful complication by meticulous monitoring of patient profile and symptomatology at every clinical visit. We conducted a prospective observational study of all patients presenting with PVT. Patients with prosthetic valve thrombosis were diagnosed based on standard criteria and clinical characteristics, risk determinants, treatments, and outcomes were assessed. Material and MethodsThis was a prospective observational study conducted in a tertiary care institute, The study was duly approved by the institutional review board and ethical committee.Inclusion Criteria All consecutive eligible participants consenting to participate suspected of having prosthetic valve dysfunction based on clinical, echocardiographic, and fluoroscopic findings would be screened for enrollment in the study.Exclusion CriteriaPatient not consenting to participate in the study.Definition Of PvtIt was defined on 3 criteria; Clinical, Echocardiographic and Fluoroscopic. A.Clinical Criteria:1)Shortness of breath 2)Features
of systemic embolization.B.Echo Criteria1)Increased gradients when compared with the reference values. 2)Prosthetic valve thrombus was recognized as soft and homogeneous, mobile or fixed echo densities located at the valve occluder and/or valve struts. The largest diameter of the thrombus as well as the length of the mobile portion, if present was measured.3)A diagnosis of pannus formation was made when fixed, bright echo dense structures, sometimes containing focal calcific deposits, were present primarily along the valve ring with extension into the valve oriC.Fluoroscopic CriteriaEach prosthesis was viewed in multiple projections including caudocranial angulations, which allowed proper visualization of prosthesis leaflet motion; that opening and closing angles were calculated. A short cine fluoroscopic film( usually 3 to 10 cardiac cycles) at 50 frames/s was recorded.Response to TreatmentComplete Response - Complete success was defined as normal or near-normal transvalvular gradient and restoration of normal leaflet motion on fluoroscopy without any major complications and clinical improvement in symptomsPartial Response - Partial success was defined as a reduction of > 50% of transvalvular gradient from the baseline or complete hemodynamic response with major complication or restricted movement of prosthetic valve leaflets on cine fluoroscopy even though the transvalvular gradients completely normalized. Failed Treatment - Failure of TT was defined as no hemodynamic response even with extended thrombolysis (up to 72 h) or death by major complications.Predefined Complications :•All-cause in-hospital mortality.•Non- fatal minor complications-bleeding without need for transfusion; TIA.•Non-fatal major complications-ischemic stroke, ICH, embolism(coronary or peripheral), bleeding requiring transfusion.Various Treatment Regimes for Thrombolytic Agents:1.Streptokinase regimen- 2.5 lakh IU intravenous bolus for 30 minutes followed by slow intravenous infusion at the rate of 1 lakh IU/hr2.Tenecteplase -slow intravenous infusion for 0.5mg/kg as an intravenous infusion for up to 72 hours in failed cases.3.Alteplase- slow intravenous infusion of 0.5mg/kg/hr.Response to Treatment :1.Serial echocardiography - Bedside echocardiography was done every six hours and gradients and valve area was recorded2.Serial fluoroscopy was done every 12 hours and opening and closing angles were determined.Once the complete response was achieved, infusion of thrombolytic agents was stopped or was continued till 72 hours in cases of failed or partial response. Premature cessation of thrombolytic therapy was done in cases of non-fatal minor or major bleeding. After successful thrombolysis, injection of low molecular heparin was given subcutaneously in doses of 1 mg/kg bid. Acenocoumarol was initiated. Both low molecular weight heparin and acenocoumarol were continued till PT/INR achieved a therapeutic range of 2.5-3.5.Non-Compliance To Treatment1. Regular - patient taking drugs(especially acenocoumarol) daily without fail.2. Irregular- taking drugs for less than five days a week for the past two days.3. Stopped- not taken drugs for last one week.Statistical Analysis Data collected were entered into a Microsoft Excel worksheet and analyzed statistically by using Statistical Package for Social Sciences (SPSS Inc., Chicago, IL). Data were presented as mean, standard deviation, and percentages.Results29 patients were diagnosed with prosthetic valve thrombosis during the study period. Table 1. Shows the clinical characteristics of the patients. The mean age of patients was 46.6±13.6 with an age range of 20-80 years. 59% of patients were females and the majority of patients 82.7% belonged to rural areas, literacy rate was 34.48%. 93.1% of the patients developed
thrombosis after more than one year of valve surgery. Thrombosis of the mitral valve was seen in 65% of patients,28% developed thrombosis of the aortic valve and 2 patients had thrombosis of the tricuspid valve. All the valves were bileaflet tilting disc type. Dyspnoea was the presenting complaint in all the patients. 23(79.3%) patients presented with NYHA class III symptoms,4(13.8%) presented with NYHA class IV, and 2(6%) presented with class II symptoms. A suboptimal therapeutic international normalized ratio was found in 86 % of valve thrombosis. NYHA: New York Heart Association, INR: international normalized ratio. Most of the patients had defaulted on their consumption of oral anticoagulant drugs.16(55%) patients were irregular in drug intake and 6(21%) had completely stopped taking medications. The most common reason for drug default was non-availability in 13 (60%), inaccessibility in 6 (27%), and ignorance in 3 (13%)(Table 2).22(76%) patients were treated with thrombolytic therapy,7(24%) patients received Heparin and intensification of anticoagulation. Streptokinase was used as a thrombolytic agent in 18 (82%), tenecteplase, and Alteplase in 2 patients each.12(66.6%)patients who received thrombolysis with streptokinase had a complete response, 4(22.3%) had a partial response and 2 patients had no response to treatment. Alteplase and Tenecteplase were used in 2 patients. The opening angle and closing angle of the aortic valve were 48.1±5.4 and 104 .1±5.5 pre thrombolysis and 10.7±0.8 and 120.8±3.6 respectively post successful lysis. The opening angle and closing angle of the mitral valve were 48.7±6.2 and 104.3±4.5 pre thrombolysis and 10.9±0.8 and 119.7±1.3 respectively post successful lysis. (Table 3) The average mean gradient across stuck aortic valve before thrombolysis was 45.5±3.2 and stuck mitral valve was 15.9±4.1. Post successful fibrinolysis, the mean gradient across the aortic valve was 20.5±1.0 and mitral valve 4.0±1.1(Table 4)8(62%) patients had complete clinical success,7(24%) had a partial response to treatment, and 4(14%) had no response to thrombolytic therapy. Duration of therapy was 24hrs in 11 patients ,18hrs in 8 paients and 72hrs in 3 patients. 3 patients succumbed to complications, one had massive ICH, and 2 had progressive heart failure. Minor bleeding was seen in 4 patients.DiscussionValvular heart diseases affect more than 100 million people around the globe and are associated with significant mortality and morbidity[3]. Obstruction to prosthetic heart valve could be due to thrombus, pannus formation, vegetation, or patient prosthesis mismatch, Prosthetic Valve thrombosis (PVT) is a pathological entity characterized by thrombus formation on the prosthetic structures, with subsequent PV dysfunction with or without thromboembolism (TE)[6-8]. There is a high prevalence of rheumatic heart disease in young in India and the majority undergo valve replacement surgery at a young age compared to developed countries [9,10]. The mean age of our patients was 46.62±13.6.most of the studies from the Indian continent of PVT belonging to younger age group in 3rd and 4th decade and female dominance [11-15]. Mean age was 58±12 in a study from Montreal [16]. The majority of patients belonged to rural backgrounds and have poor availability of health resources and medical care. This might contribute to drug default by the patient. The majority of patients in our study group were illiterate which might contribute to ignorance which further lead to failure in regular drug intake and cause them to default the drug regimen. Poor drug compliance also emerged as a significant risk factor in studies done by Durrleman et al reported 10 out of 39 were defaulters and Manjula et al reported 23 out of
26 patients were non-compliant [16,17]. The majority of studies have cited sub-therapeutic INR as a major risk factor for the development of PVT which was mainly due to irregular follow-up and poor treatment compliance. Studies from India show variable rates of inadequate anticoagulation ranging from 41.5 To 90.3% [18-20]. Egbe et al found inadequate anticoagulation in 48% of patients with PVT [21].All patients of PVT presented with dyspnea and a muffled click on examination. The most common presentation is dyspnoea in the majority of studies. Most of the patients presented with NYHA class III and Class IV symptoms In our series, most patients were in NYHA class III at presentation (79.3%) whereas in series by Nawale et al. maximum patients fell under NYHA class IV (52.4%)[14]. In the series by Durrleman et al, they reported the maximum number of patients were in class III or IV at presentation (87%)[16]. Similarly in the study published by Gupta et al, reported that 46.4% of patients were in NYHA class III and 24.5 % of patients were in NYHA class IV at the time of presentation[18]
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