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Introduction: Presently off- pump CABG has proved itself tobe a safe, cheaper and effective alternative of on- pump CABG.However, it requires manipulation, displacement, positioning& mechanical stabilization of the heart during grafting whichmay cause haemodynamic alteration. Study was done withthe objective of finding out the changes in Central VenousPressure (CVP); Mean Arterial Pressure (MAP); MeanPulmonary Arterial Pressure (MPAP); Right Ventricular EndDiastolic Pressure (RVEDP) & Left Ventricular End DiastolicPressure (LVEDP) while grafting the anterior, lateral &inferior surfaces of heart during off-pump CABG.Material and methods: Over one year time, 50 patients withLVEF ≥40%, undergoing off-pump CABG were monitoredfor the above parameters at various stages of their operation,namely:- 1. During manipulation & shunt introduction,2.During anastomosis without shunt, 3.During anastomosiswith shunt & 4.After anastomosis; while grafting the anterior,lateral & inferior surfaces of heart. These results werecompared with the baseline values of CVP, MAP, MPAP,RVEDP & LVEDP, to look for statistical significance.Results: During manipulation & shunt introduction; CVP(mmHg) significantly increased during Ramus grafting - 12±1.8(p<0.047); and also during OM grafting – 12.6±1.9 (p<0.045),when compared to a baseline value of 9±1.8. The MAP(mmHg) was significantly decreased during manipulation &shunt introduction in Diagonals - 70±5.8 (p<0.046), Ramus- 70±5.8 (p<0.048), OMs - 65±5.8 (p<0.028) & in the Rightterritory - 69±5.9 (p<0.032); as compared with baselineMAP of 76±11.7. During anastomosis without shunt also, theMAP(mmHg) significantly decreased while grafting LAD- 70±3.8 (p<0.048), Diagonals - 68±3.8 (p<0.039), OMs –71.8±4.8 (p<0.039) & Right sided arteries 70.8±4.6 (p<0.039),as compared with baseline MAP values. The MPAP(mmHg)was significantly increased – 18.3±3.7 (p<0.047) as comparedto the baseline value of 16±2.4 during manipulation & shuntintroduction in the OMs.Conclusion: During OPCABG there will be significantalterations in haemodynamics mostly due to mobilizationof the heart, which is necessary to visualise the targetvessels properly & stabilisation of the concerned areawith stabiliser. However, by observing the haemodynamicvariations constantly & by making necessary mechanical &pharmacological adjustments, unnecessary conversion to Onpump technique can be avoided.
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Pulmonary hypertension (PH) is a devastating disease caused by different etiology and characterized by the progressive elevation of pulmonary vascular resistance and pulmonary artery pressure. As a new method that applied to clinical studies, computational fluid dynamics (CFD) gradually becomes a powerful tool for in-depth understanding of the disease progression. It can noninvasively obtain the patient-specific hemodynamic parameters at any point of the vessel and present them through the visualization technology. In this paper, an overall review of CFD with the focus on PH, including the numerical simulation method, boundary conditions, blood characteristics and relevant hemodynamic parameters was presented.
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Introduction: Pulmonary artery hypertension (PAH) whichcan be primary or secondary, has been found to be associatedwith chronic kidney disease, especially end stage renal disease.Finding prevalence of pulmonary hypertension in early stagesof chronic kidney disease is important because it createsvery high burden of cardio vascular morbidity and mortality.In this study we have assessed various factors associatedwith prevalence of pulmonary hypertension in patients withglomerular filtration rate less than 30ml/min per 1.73 metersquare on dialysis.Material and methods: This is a one year, hospital based,prospective observational study of patients aged more than 18years with GFR less than 30 ml/min per 1.73-meter square ondialysis, who were found to have pulmonary hypertension onechocardiography. The prevalence of pulmonary hypertensionin this group of patients and the risk factors in CKD associatedwith it are calculated followed by a descriptive analysis andinterpretation of the data.Results: The various factors we analyzed and p value forassociation of pulmonary hypertension in CKD for thepercentage of male and female in our study group is 0.241, fordistribution of the pulmonary hypertension among differentage groups is 0.503, for the significance of diabetic mellitus is0.595,for systemic hypertension is 0.206, for arterial venousfistula is 0.780,for superimposed infections 0.166, for volumeoverload is 0.560, for anemia is 0.780, for left ventriculardiastolic dysfunction is 0.662, for creatinine clearance is0.717,for duration of dialysis is 0.000. With above results,only association with significant p-value (0.000) in our studypopulation with pulmonary hypertensions longer duration.Conclusion: Prevalence of pulmonary hypertension in ourstudy is 22%. The risk factors like age,sex, diabetes, systemichypertension, AVF, superimposed infection, volume overload,anaemia, LVDD has no influence on pulmonary hypertensionin our study, only strong association that we have in our studypopulation with pulmonary hypertension with CKD is longerduration of dialysis.
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Background: Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) has considerable cardiovascular risk. Various cardiovascular diseases are common during exacerbations. Both diseases share several similarities such as older age of the patient, smoking as a common risk factor and symptoms of exertional dyspnea. Knowledge regarding the magnitude of underlying cardiovascular diseases during AECOPD is limited. Authors performed this study to assess the presence of different associated cardiovascular diseases (CVDs) in patients hospitalized for AECOPD and its effect on the outcome.Methods: It was a prospective observational study involving 436 patients of AECOPD divided to Group 1 (AECOPD with CVD- 137 (31.4%) patients) and Group 2 (AECOPD without CVD 299 (68.6%) patients). All the patients were subjected to full history taking, clinical examination, chest X-ray, spirometry, ECG and echocardiography.Results: COPD patients in exacerbation with CVD, were significantly more likely to have longer duration of hospital stay (p < 0.0001), high CRP level (p<0.001), more frequent mechanical ventilations (p < 0.001), two or more exacerbations per year (p <0.0001) and the mortality was (p<0.0001). Also, they have GOLD grade III/IV severe (43.5%) and very severe (19.5%) air flow limitation. The high percentage of them had (64.8%) pulmonary hypertension, (37.3%) systemic arterial hypertension, (31.5%) arrhythmia, (27.8%) ischemic heart diseases and (21.3%) heart failure.Conclusions: The prevalence of cardiovascular diseases (CVD) in patients hospitalized for COPD was high. Age, sex and CVD trends, as well as life style changes, should be considered when prevention and control strategies are formulated.
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Objective: To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods: Twenty patients with simple ventricular septal defect (VSD) were chosen as controls, and 30 patients with PH were studied. Plasma levels of ET-1 and NO were measured by radioimmunoassay or colorimetric method. Before cardiopulmonary bypass was established, the specimens from right lung were fixed with formaldehyde solution, embedded with paraffin and stained by SP immunohistochemistry. Intercellular adhesion molecule-1 (ICAM-1) expression was measured through the determination of the light density with computer imaging technology. Results: Compared with that of the patients with simple VSD, the light density of ICAM-1 and plasma level of ET-1 increased in patients with PH; but plasma level of NO decreased (P<0.05). Positive correlation was observed between ICAM-1 and ET-1/NO (P<0.05). Conclusion: Endothelia cells activation and imbalance of ET-1/NO might play an important role in the development of PH.
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Objective To explore the correlation between endothelia cells activation and cytokines (ET-1, NO) levels in patients with pulmonary hypertension (PH), and to discuss their roles in the development of PH. Methods Twenty patients with simple ventricular septal defect (VSD) were chosen as controls, and 30 patients with PH were studied. Plasma levels of ET-1 and NO were measured by radioimmunoassay or colorimetric method. Before cardiopulmonary bypass was established, the specimens from right lung were fixed with formaldehyde solution, embedded with paraffin and stained by SP immunohistochemistry. Intercellular adhesion molecule-1 (ICAM-1) expression was measured through the determination of the light density with computer imaging technology. Results Compared with that of the patients with simple VSD, the light density of ICAM-1 and plasma level of ET-1 increased in patients with PH; but plasma level of NO decreased (P<0.05). Positive correlation was observed between ICAM-1 and ET-1/NO (P<0.05). Conclusion Endothelia cells activation and imbalance of ET-1/NO might play an important role in the development of PH.
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Objective To study the relationship between TXA 2/PGI2 and pulmonary hypertension in Congenital Heart Disease(CHD).Methods The serum concentration of TXB2/6-K-PGF1? was determined in 63 patients with CHD by radioimmunoassay. Results TXB2 ，TXB2 /6-K-PGF1? increased significantly in P H,while 6-K-PGF1? decreased,the TXB2 /6-K-PGF1? varied in different PH groups(P＜0.05).Conclusion TXA2/PGI2 plays an important role in the pathogenesis of PH se- condary to CHD.
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The electromicroscopic observation of atrialbiopsy was carried out in 10 patients with ventric-ular septal defect (VSD) and middle, severe pul-monary hypertension (PH). The observation sug-gests that there are myofibrillar lysis to disappearwith various degrees, dilated rough endoplasmreticulum and the increase in lipofuscin granulesand lipid droplets; mitochondral hyperplasia, theirsize and shape being different, disorganizing of mi-tochondria, disintegration of cristae, mitochondralretrograde degenration and decreased matrix elec-tron density. The dilated intercalated discs and in-crease in myocardial fibrous tissue were found inpart of patients. These structural changes areprobably due to chronic myocardial ischemia.
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We find that there is a correlation among thesize of ventricular septal defect (VSD) (X_2), PaO_2(X_3), V. /V. (X_7) and pulmonary systolic pressure(Y_1), diastolic pressure (Y_2), mean pressure (Y_3)by multivariate stepwise regression analysis, andso there are their parameters in the regression e-quations. The regression equations are Y_1 = 13. 24+ 0. 22X_2 - 0. 09X_3 + 0. 14X_7; Y_2 = 0. 65 + 0. 24X_2+ 0. 12X_7; Y_3 = 3. 54+ 0. 17X_2 + 0. 16X_7. But thecourse of the disease, ∑9 leads QRS dimension,R. /R., L. /L. are non-dominant factors, and sothere are not their parameters in the regression e-quation. The above-mentioned equations mayavoid the patients. with mild, moderate pulmonaryhypertension to have invasive examination, and re-duce its complications.