Chronic Rheumatic Mitral Stenosis Research Articles

Comparison of the Appendicular Emptying Velocity of Left Atrium in patient with moderate versus severe chronic rheumatic mitral stenosis measured by pulsed wave Doppler in Transesophageal echocardiography

Background: Left atrial appendage (LAA) is considered the “most lethal human appendage” as it causes significant mortality and morbidity in chronic rheumatic mitral stenosis patients due to cardiogenic cerebral infract. Presence of LAA dysfunction has been shown to be a strong predictor of thrombus formation and the risk of embolic event, even if no clot is found at the time of initial examination. LAA emptying velocity are measured by trans esophageal echocardiography (TEE) represent as a surrogate marker for left atrial(LA) function .LAA emptying velocities (contraction velocity) < 20cm/s are associated with risk of spontaneous echo contrast(SEC), LAA thrombus, and subsequent cardio embolic events. So early detection of low emptying velocity without SEC or LA thrombus can reduce mortality & morbidity related to cardio embolic stroke and also helps in further management procedure like cardio version etc. So we will compare LAA emptying velocity moderate versus severechronic rheumatic mitral stenosis patients in our population for further attention.
 Objective: To assess emptying velocity of LAA in patient with moderate versus severe chronic rheumatic mitral stenosis, from a Bangladesh health service perspective.
 Method: This was a cross sectional study which was conducted in UCC, BSMMU during the period of from February 2019 to September 2019 in Echo lab .
 Study Procedure: We were enrolled 33 CRHD with MS (moderate to severe) patients who underwent TEE and met inclusion & exclusion criteria. The purpose of the study was explained to each subject & informed written consent was obtained. After getting consent relevant history, physical examination and preprocedural investigation was obtained in predesigned structured data collection sheet. TEE was done with Vivid E9® machine. Pulse wave Doppler was position at the tip of the LAA and then emptying velocity of LAA moderate and severe were compared.
 Outcome measure: Among 33 patients, 3 patients were excluded due to outlier and inadequate data.. In chronic rheumatic mitral stenosis in moderate versus severe cases average LAA emptying velocities were significantly higher moderate CRHD with MS compare to severe CRHD with MS,(26.57±4.91;31.12±5.04), P=0.018.
 Conclusion:Appendicular emptying velocity of LAA significantly lower in severe CRHD with MS compare to moderate CRHD with MS and it has temporal relation with MS severity. It can be used as a reliable, simple and sami-invasive tool to early predict severity and prevent complication in CRHD with MS as well as for prophylactic measured taken.
 University Heart Journal 2022; 18(2): 73-79

Tricupsid valve involvement in chronic rheumatic mitral stenosis: An observational study.

Objective: The aim of this study was to assess the incidence of tricuspid valve involvement in rheumatic mitral stenosis among Pakistani patients that helps in the medical decisions and special consideration for the management of disease. Study Design: Prospective Study. Setting: National Institute of Cardiovascular Disease (NICVD), Karachi. Period: February 2018 to November 2019. Material & Methods: As per the study inclusion criteria, Three fifty eight (358) Pakistani patients' diagnosed with Rheumatic Mitral stenosis. The study was compiled as per international standards (ICH-GCP-E6), prior to initiation, the ethics review committee approved the study and informed consent was taken from all recruited subjects. Results: The study prospectively assessed the echocardiographic profile of rheumatic heart disease patients and recruited 358 patients with chronic Rheumatic Mitral Stenosis. Out of these patients, 93.9% (336) had tricuspid regurgitation and 7% (25) had triscuspid stenosis. Their ages ranged from 14 to 85 years (mean 40.3 years). Of these, 73.6% (263) were females and 26.5% (95) were males. On the basis of severity, in case of tricuspid stenosis, 3.9% (14) were mild, 1.1% (4) were moderate and 2% (7) were progress from mild to moderate. In case of Tricuspid regurgitation, 39.9% (143) were mild, 29% (105) moderate and 88% (24.6) were severe. Conclusion: The study concluded that in the local population, the patients with chronic Rheumatic Mitral Stenosis had common involvement of Triscuspid valvular disease, more come in female and affected all age groups. Hence, before management of Rheumatic Mitral Stenosis with other lesions, especially the Triscuspid valve involvement, detailed assessment is required in order to achieve the best outcome in patients with the Mitral valve disease.

223 Association of levels of IL-6, IL-10, IL-18 and TNF-alpha with rheumatic mitral stenosis and subsequent pulmonary hypertension

Abstract Background Rheumatic heart disease (RHD) remains a serious public health problem in developing countries. The pattern of immune response after exposure to streptococcal infection is one of the main determinants of the rheumatic inflammatory process, making it essential to identify the patients who have a higher risk of disease progression. Objective To give an insight into the pathophysiology of the rheumatic afflicted valves and the role of IL-6, IL-10, IL-18 and TNF-α in the different stages of RHD. Methods The study included 84 consecutive patients (62 females, mean age 34.6 ± 10.6 years) with symptomatic, severe chronic rheumatic mitral stenosis (Group-A). 79 age and gender matched normal healthy volunteers were enrolled as controls (Group-B). Patients with chronic rheumatic mitral stenosis were further divided into subgroups based on severity of mitral stenosis [MVA ≤ 1 cm2 (Subgroup Aa) and MVA > 1 cm2 (Subgroups Ab)] and presence or absence of pulmonary hypertension [RVSP ≥ 36 mm Hg (Subgroup Ac) and RVSP < 36 mm Hg (Subgroup Ad)]. IL-6, IL-10, IL-18, TNF-α and hs-CRP levels were assessed in both groups. Results The mean serum levels of IL-6, IL-10, IL-18, TNF-α and hs-CRP in Group-A and Group-B were 6.57 ± 3.53 pg/mL and 2.73 ± 1.01 pg/mL (p <0.001), 8.19 ± 2.80 pg/mL and 3.51 ± 0.86 pg/mL (p <0.001), 136.31 ± 89.02 pg/mL and 47.96 ± 9.76 pg/mL (p <0.001), 21.26 ± 18.59 pg/mL and 5.36 ± 3.57 pg/mL (p <0.001), 4.69 ± 6.31 pg/mL and 2.63 ± 2.22 pg/mL (p <0.008) respectively. On subgroup analysis mean TNF-α in subgroup Aa was 20.71 ± 16.84 pg/mL, while in subgroup Ab it was 7.56 ± 1.93 pg/mL (p <0.001). Mean IL-10 in subgroup Ac and Ad was 8.74 ± 3.29 pg/mL and 7.47 ± 1.82 pg/mL respectively (p <0.028). Conclusions Chronic rheumatic mitral stenosis patients have increased IL-6, IL-10, IL-18, TNF-α and hs-CRP levels suggesting a continuous ongoing inflammatory activity even in chronic phase. Further subjects having severe mitral stenosis had increased TNF-α levels in comparison to subjects with mild to moderate mitral stenosis suggesting its possible role in acceleration of rheumatic process. Cytokines in various subgroup Parameter IL-6 (pg/ml) p IL-10 (pg/ml) p IL-18 (pg/ml) p TNF-α (pg/ml) p hs-CRP (pg/ml) p Subgroup Aa 5.63 ± 3.25 0.13 8.38 ± 3.06 0.32 146.35 ± 103.84 0.20 20.71 ± 16.84 <0.001 3.72 ± 3.43 0.67 Subgroup Ab 6.90 ± 3.57 7.72 ± 2.04 112.28 ± 22.79 7.56 ± 1.93 4.27 ± 3.81 Subgroup Ac 6.86 ± 3.50 0.44 8.74 ± 3.29 0.02 145.29 ± 103.01 0.29 20.25 ± 17.02 0.53 4.77 ± 0.93 0.93 Subgroup Ad 6.21 ± 3.49 7.47 ± 1.82 124.67 ± 66.95 22.91 ± 20.68 4.66 ± 3.44 Abstract 223 Figure. Cytokines in case and control

Main pulmonary artery aneurysm with chronic rheumatic mitral stenosis: a case report

Pulmonary artery aneurysm associated with chronic rheumatic heart disease has not been reported. Isolated aneurysmal dilatations of pulmonary artery of varying etiology occur, not infrequently. Cystic medial necrosis as a cause of main pulmonary artery aneurysm has been cited quite often. We report a 48-year-old female with main pulmonary artery aneurysm of size 8.1 cm associated with chronic rheumatic mitral stenosis. Aneurysmorrhaphy and mitral valve replacement were done successfully. Histopathology of main pulmonary artery wall was consistent with cystic medial necrosis wherein in same patient the excised mitral leaflets showed the evidence of chronic rheumatic heart disease (hyaline degeneration).

Proteomic analysis of human plasma in chronic rheumatic mitral stenosis reveals proteins involved in the complement and coagulation cascade.

BackgroundRheumatic fever in childhood is the most common cause of Mitral Stenosis in developing countries. The disease is characterized by damaged and deformed mitral valves predisposing them to scarring and narrowing (stenosis) that results in left atrial hypertrophy followed by heart failure. Presently, echocardiography is the main imaging technique used to diagnose Mitral Stenosis. Despite the high prevalence and increased morbidity, no biochemical indicators are available for prediction, diagnosis and management of the disease. Adopting a proteomic approach to study Rheumatic Mitral Stenosis may therefore throw some light in this direction. In our study, we undertook plasma proteomics of human subjects suffering from Rheumatic Mitral Stenosis (n = 6) and Control subjects (n = 6). Six plasma samples, three each from the control and patient groups were pooled and subjected to low abundance protein enrichment. Pooled plasma samples (crude and equalized) were then subjected to in-solution trypsin digestion separately. Digests were analyzed using nano LC-MSE. Data was acquired with the Protein Lynx Global Server v2.5.2 software and searches made against reviewed Homo sapiens database (UniProtKB) for protein identification. Label-free protein quantification was performed in crude plasma only.ResultsA total of 130 proteins spanning 9–192 kDa were identified. Of these 83 proteins were common to both groups and 34 were differentially regulated. Functional annotation of overlapping and differential proteins revealed that more than 50% proteins are involved in inflammation and immune response. This was corroborated by findings from pathway analysis and histopathological studies on excised tissue sections of stenotic mitral valves. Verification of selected protein candidates by immunotechniques in crude plasma corroborated our findings from label-free protein quantification.ConclusionsWe propose that this protein profile of blood plasma, or any of the individual proteins, could serve as a focal point for future mechanistic studies on Mitral Stenosis. In addition, some of the proteins associated with this disorder may be candidate biomarkers for disease diagnosis and prognosis. Our findings might help to enrich existing knowledge on the molecular mechanisms involved in Mitral Stenosis and improve the current diagnostic tools in the long run.Electronic supplementary materialThe online version of this article (doi:10.1186/1559-0275-11-35) contains supplementary material, which is available to authorized users.

Comparison of inflammatory marker levels in atrial fibrillation and sinus rhythm in patients with chronic rheumatic mitral stenosis

Purpose: Studies have shown that Atrial fibrillation (AF) associated with rheumatic mitral stenosis (MS) is not invariably linked to severity of stenosis. We hypothesized that continuing low-grade inflammation may be the causative factor for AF in rheumatic MS. Methods: 65 patients of severe rheumatic MS (Mitral Valve area of less than 1.0 cm2) were studied. Patients with acute rheumatic activity, an active infective process and more than mild involvement of other valves were excluded. Patients in normal sinus rhythm (NSR) were subjected to 24 hour holter analysis to detect paroxysmal AF. The patients were studied in three groups; NSR (group A), paroxysmal AF (group B), and permanent AF (group C). Level of inflammatory biomarkers hs-CRP, IL-6 and sCD-40L were measured in the three groups. Results: Mean age was 33.83±8.03 years. There were 24, 12 and 29 patients respectively in Groups A, B and C. 10 healthy volunteers served as controls. Levels of hs-CRP were elevated ≥6mg/dl in 2 patients (8.33%), 1 patient (8.33%) and 11 patients (37.93%) in groups A, B and C respectively and in none of the controls. CRP levels were significantly higher in group C as compared to group A (p=0.013). sCD-40 level was 2.23±1.732 ng/dl in normal population, while it was 3.90±2.64, 3.46±3.24 and 4.84±3.80ng/dl in group A, B and C respectively.(p=NS). IL-6 levels showed graded increase across the groups. Level in controls was 1.36±1.25 mg/dl, while group A, B and C had levels at 1.40±1.69, 2.97±5.76 and 5.41±7.48 mg/dl respectively. The difference was statistically significant between group A and C (p=0.005). Conclusion: Levels of hs-CRP and IL-6 were selectively elevated in patients of Rheumatic severe MS with AF as compared with those in NSR. This suggests that inflammation may play a role in the pathogenesis of AF in RHD independent of valve severity.

Elevated platelet microparticle levels in valvular atrial fibrillation

Platelet activation occurs in peripheral blood of patients with rheumatic mitral stenosis (MS) and atrial fibrillation (AF) and could be related to abnormal thrombogenesis. However, the plasma level of platelet microparticles (PMPs), a marker of platelet activation, in patients with valvular AF remains unresolved. We performed a case control study of 20 patients with chronic rheumatic MS and chronic long AF and 10 healthy volunteers who were in sinus rhythm. Peripheral plasma levels of PMP were assessed by quantifying CD41-positive microparticles by flow cytometry. The mitral valve area was calculated by means of the Doppler pressure half-time method. The levels of circulating PMP were elevated significantly in valvular AF patients when compared with controls (12·36±5·51 × 105/ml versus 7·56±0·86 × 105/ml, P=0·011). Correlation analysis demonstrated that there was a significantly direct relationship between the severity of MS and PMP levels (r=−0·507, P=0·004). We conclude that in patients with rheumatic MS and AF, there is evidence of platelet activation detected by high PMP levels which have a significantly direct relationship with the severity of MS.

High levels of high sensitivity C-reactive protein predict the progression of chronic rheumatic mitral stenosis

High sensitive C-Reactive Protein (hs-CRP) predicts morbidity and mortality in various clinical conditions. The effect of hsCRP on progression of chronic rheumatic mitral stenosis (CRMS) has not been demonstrated. A total of 132 patients with CRMS (95 female, 37 male) and 145 control (100 female, 45 male) were included in the study. Baseline clinical, echocardiographic, hematologic and hs-CRP measurements were collected prospectively. Mean mitral valve area (MVA) was 1.4 +/- 0.3 cm(2), mean wilkins valve score value was 8.9 +/- 1.7, left atrial diameter was 5.0 +/- 0.7 cm, left atrial area was 37.2 +/- 12.6 cm(2), and systolic pulmonary arterial pressure (SPAP) was 44 +/- 11 mmHg in patients with CRMS. The mean levels of hs-CRP value, fibrinogen, and mean platelet volume (MPV) were significantly higher in CRMS group compared to control group. The levels of hsCRP were found to be positively correlated with mean Wilkins valve score value, SPAP, presence of atrial fibrillation (AF), left atrial diameter, left atrial area, presence of LASEC(+), fibrinogen, and MPV and inversely correlated with MVA in patients with CRMS. Linear regression analysis revealed that the hsCRP level independently affects mean Wilkins valve score value, left atrial area (LAA), LASEC(+) and AF in the patients with CRMS. These results suggest that increased hsCRP levels are associated with CRMS severity. These association may be important when treating patients with CRMS.

Isolated left ventricular noncompaction in association with rheumatic mitral stenosis

Fifty year old man with a known case of chronic rheumatic heart disease with atrial fibrillation was presented with severe mitral stenosis. He was incidentally detected to have noncompaction of left ventricle on echocardiography and Doppler examination. He underwent successful percutaneous trans-luminal mitral commissurotomy (PTMC) for severe mitral stenosis. This is the first reported case of isolated ventricular noncompaction (IVNC) associated with acquired chronic rheumatic mitral stenosis.

Comparison of mitral valve area, pulmonary function and pulmonary artery hypertension in patients with chronic rheumatic mitral stenosis undergoing surgical closed mitral valvotomy (SCMV) versus percutaneous balloon mitral valvotomy (PBMV)

Comparison of mitral valve area, pulmonary function and pulmonary artery hypertension in patients with chronic rheumatic mitral stenosis undergoing surgical closed mitral valvotomy (SCMV) versus percutaneous balloon mitral valvotomy (PBMV)

Lambl's excrescences inside the left ventricle due to rheumatic mitral stenosis

A patient with chronic rheumatic mitral stenosis had Lambl's excrescences at the site where the jet of blood through the stenotic mitral orifice impinged on the interventricular septum. There is dispute whether Lambl's excrescences are neoplastic or related to chronic trauma. The present case adds credence to the latter view.

Papillary muscle hypertrophy in chronic rheumatic mitral valve stenosis. A clinicopathologic study.

A quantitative pathologic study was performed on papillary muscles in 15 cases of chronic rheumatic mitral stenosis. The papillary muscles were grossly hypertrophied as compared with papillary muscles in 10 normal specimens. Hypertrophy of papillary muscles was associated with pronounced fibrosis. Angiographically, these hearts were remarkable in small left ventricular cavity with almost complete cavity elimination at end systole. Left ventricular wall dyskinesia was also present. It is probable that derangement of the mitral valve structure due to rheumatic process leads to more stress on the supporting elements, thus resulting in papillary muscle hypertrophy.

HIS bundle electrogram in rheumatic mitral valve disease with special reference to Bachmann's bundle block in P mitrale.

HBEs were recorded from either the right or left ventricle or simultaneously from both in 26 patients with chronic rheumatic mitral stenosis alone or in association with other mild valvular lesions during the diagnostic cardiac catheterization. Eleven of the patients had auricular fibrillation. Of the remaining 15 patients with sinus mechanism and P mitrale in the surface electrocardiogram, 12 were noted to have H potential preceded the termination of P wave and gave P2H interval of negative value- so-called "Bachmann's bundle block". Among these, double atrial activities (A and A' waves) could be identified on the HBE recorded from the left ventricular endocardial surface with catheter electrodes positioned at the subarotic region in 7 patients studied. Interatrial conduction time (P1A' interval) measured in these patients was prolonged in all and ranged from 47 to 82 with an average of 66 msec. Prolongation of intraatrial (or internodal) conduction time was noted in only one patient who also had first degree A-V block and prolonged A-H interval. There was no correlation of either P1P2 or P2H interval to the degree of left atrial enlargement. The P1P2 or P2H interval also had no correlation with hemodynamic parameters. In patients with auricular fibrillation, all impulses unable to conduct to the ventricle were blocked proximal to the His bundle and concealed conduction was not observed distal to it.