Impact of pulmonary hypertension on early outcomes of valve surgery in rheumatic heart disease: The first outcome-based study from Yemen.

AimMitral valve pathology in rheumatic heart disease patients is a common cause of secondary pulmonary hypertension (PH). Our aim was to evaluate pulmonary hypertension severity as a predictor of in-hospital mortality and early complications following mitral valve replacement.MethodsA retrospective review of rheumatic heart disease patients who underwent mitral valve replacement between January 2017 and August 2020 was performed. Systolic pulmonary artery pressure (sPAP) was used to classify patients as no PH (<35 mmHg), mild PH (35-44 mmHg), moderate PH (45-59 mmHg) or severe PH (>60 mmHg). Patients subjected to additional cardiac procedures (such as aortic valve replacement and coronary artery bypass grafting) were excluded from the study sample.ResultsThe study group was composed of 159 patients (mean age: 40; 73 male, 86 female) categorized as no PH (n = 32; 20.1%), mild PH (n = 14; 8.8%), moderate PH (n = 65, 40.9%) and severe PH (n = 48, 30.2%) groups. Patient demographic data and preoperative comorbidities were comparable among the four groups. Use of intraoperative and postoperative blood products was similar in all the groups. Severe PH patients had similar in-hospital mortality (4.2%; p = 0.74) as in groups with lesser degrees of pulmonary hypertension. Likewise, increasing severity of pulmonary hypertension did not confer any significant increase in early postoperative complications, namely prolonged ICU stay (10.4%; p = 0.41), prolonged ventilation (2.1%; p = 0.70), reintubation (4.2%; p = 0.90), reopening for bleeding tamponade (6.3%; p = 0.39), new-onset renal failure (6.3%; p = 0.91), postoperative stroke (4.2%; p = 0.52) or prolonged length of stay (mean: 5.6 + 2.8 days; p = 0.49).ConclusionsIncreasing severity of pulmonary hypertension does not appear to have a significant impact on in-hospital mortality or early postoperative outcomes of patients undergoing mitral valve replacement.

To investigate clinical value of Tei index used for monitoring right ventricular (RV) function in pregnant women complicating cardiac disease accompanying pulmonary hypertension (PH) and the influence on left ventricular (LV) function due to overload pressure of RV. Fifty-eight pregnant women complicating cardiac disease (including 32 cases with congenital heart disease, 14 cases with rheumatic heart disease and 8 cases with arrhythmia) were enrolled in this study, among 26 cases coexisted with pulmonary hypertension. According to the pressure of PH, those patients were divided into three groups: 11 cases in mild group [30 - 49 mm Hg (1 mm Hg = 0.133 kPa)], 9 cases in moderate group (50 - 79 mm Hg) and 6 cases in severe group (>or= 80 mm Hg). In the mean time, 15 healthy pregnant women were matched as control. Tei index were measured for LV and RV respectively. (1) The isovolumetric relaxation time [IRT, (93 +/- 52) ms] and isovolumetric contraction time [ICT, (66 +/- 41) ms] of RV in PH group were significantly higher than normal controls [(39 +/- 19) ms in IRT and (38 +/- 20) ms in ICT] and the other patients without PH group [(59 +/- 12) ms in IRT and (43 +/- 19) ms in ICT, P < 0.01, P < 0.05; P < 0.05, P < 0.05]; however, ejection time (ET) was (239 +/- 46) ms significantly shortened in PH group (P < 0.05, P < 0.01) when compared with (250 +/- 41) ms in patients without PH and (299 +/- 38) ms in normal controls. Tei index in PH group were 0.72 +/- 0.49, which were significantly higher than 0.38 +/- 0.12 in normal controls and 0.43 +/- 0.16 in patients without PH (P < 0.01, P < 0.05). (2) The IRT [(99 +/- 27) ms] and ICT [(71 +/- 40) ms] of LV in PH group were significantly higher than in normal controls [(88 +/- 20) ms, (50 +/- 24) ms] (P < 0.01, P < 0.01). ET of LV in PH group [(202 +/- 26) ms] were significantly shortened that (290 +/- 21) ms in normal controls and (220 +/- 36) ms in patients without PH (P < 0.01, P < 0.05). Tei index of LV in PH group were significantly higher than 0.43 +/- 0.15 in normal controls and 0.58 +/- 0.21 in patients without PH (P < 0.01, P < 0.05). (3) Positive correlation between Tei index of RV and pressure of pulmonary artery were observed (r = 0.84, P < 0.01). (4) Tei index of RV in severe PH were significantly higher than mild PH (0.75 +/- 0.43 vs. 0.68 +/- 0.35, P < 0.01) and moderate PH (0.75 +/- 0.43 vs. 0.71 +/- 0.14, P < 0.05). (1) The Tei index is a novel efficient Doppler index in assessing RV function of pregnant women complicating cardiac disease accompanying PH. And the fluctuation of Tei index might reflect seriousness of the disease. (2) The overload pressure of RV pressure due to PH has significant influence on LV function.

Cardiac Anesthesiologist and Global Capacity Building to Tackle Rheumatic Heart Disease

MISSED OPPORTUNITIES AND ECHOCARDIOGRAPHIC EVIDENCE OF PULMONARY HYPERTENSION: A QUALITY-IMPROVEMENT TASK FORCE TO TRIGGER EARLY REFERRAL

Background We addressed the paucity of data describing the characteristics and natural history of incident pulmonary hypertension (PHT). Methods In this observational clinical cohort study, we examined 85,173 individuals undergoing routine echocardiography for heart disease without evidence of PHT (according to estimated right ventricular systolic pressure, eRVSP &amp;lt;30 mmHg). Subsequent age and sex-specific incidence of PHT were derived from repeat echocardiograms conducted a median of 3.43 (interquartile range, IQR 1.49 to 6.55) years apart in 13,448 adults. Progressive PHT severity with individual data linkage to all-cause mortality were examined per PHT stage: eRVSP 30–39 mmHg (mild PHT), 40–49 mmHg (moderate PHT) and ≥50 mmHg (severe PHT). Results A total of 6,169 men (45.9%, mean age 61.4±16.7 years) and 7,279 women (60.8±16.9 years) with no initial evidence of PHT were identified (first echocardiogram). Subsequently, 5,412 (40.2%,) developed PHT (repeat echocardiogram) – comprising 4,125 (30.7%, 65.0±14.3 years), 928 (6.9%, 69.2±13.5 years), and 359 (2.7%, 69.8±12.7 years) cases of mild, moderate, and severe PHT, respectively. The incidence of all stages of PHT was 15.2 cases per million men/annum and 12.5 cases per million women/annum. Overall, median eRVSP increased by +7.4 (IQR +4.6 to +10.1) and +30.7 (IQR +26.0 to +37.3) mmHg; median E:e' ratio increased by +1.0 (IQR −0.4 to +3.2) and +3.6 (IQR +2.0 to +8.2); and median LA volume increased by +5.0 (IQR +0.0 to +12.0) and +19.5 (IQR +9.0 to +31.0) ml/m2, respectively, in mild and severe PHT groups between first and last echocardiograms. During subsequent median 8.1 years follow-up, 2,776/13,448 (20.6%) individuals died from all-cause. Compared to no PHT, the age- and sex-adjusted hazard ratios for all-cause mortality increased to 1.35 (95% confidence interval, CI 1.23–1.47) in mild PHT, 1.94 (95% CI 1.73–2.18) in moderate PHT, and 2.43 (95% CI 2.09–2.83) in severe PHT (all p&amp;lt;0.001). Conclusions New onset of PHT is a common finding among individuals with heart disease followed-up with echocardiography. Even milder stage of PHT is associated with higher mortality, reinforcing the need for proactive evaluation for symptoms consistent with PHT. Funding Acknowledgement Type of funding sources: Private grant(s) and/or Sponsorship. Main funding source(s): Johnson &amp; Johnson: Investigator-initiated grant

Background: Mitral valve replacement (MVR) plays a central role in the management of patients with mitral stenosis with moderate to severe pulmonary hypertension. Pulmonary hypertension has an impact on short term outcome of MVR. It can influence left ventricular function (low output syndrome), incidence of arrhythmia, ARDS leading to respiratory failure and right ventricular failure which may be irreversible.&#x0D; Methods: The immediate postoperative hemodynamics in 40 patients with moderate to severe pulmonary arterial hypertension who underwent mitral valve replacement (BLMV) between July 2010 and June 2012 were studied prospectively. Patients were divided into two groups: Group A (n=20): Patient having MS with moderate pulmonary hypertension (PASP: 40-59 mm-Hg) and Group B (n=20): Patient having MS with severe pulmonary hypertension (PASP e” 60mm-Hg). Total two follow up were done- 1st follow up after 10 days and 2nd follow up after 1 month of MVR. Each patient was assessed by medical history, clinical examination &amp; color doppler echocardiogram.&#x0D; Results: It was shown that surgery can be beneficial for the patients if MVR is done in the state of mild PAH irrespective of age but beyond this level of PAH, the patients may still remain with mild pulmonary hypertension which may trigger the cascade of pulmonary vascular Disease may be the cause of unsatisfactory outcome. So, early surgical outcome of mitral stenosis with moderate pulmonary hypertension is better than mitral stenosis with severe pulmonary hypertension.&#x0D; Conclusion: We conclude that MVR in patients having MS with moderate PAH is a safe and effective measures for preventing pulmonary hypertension related complications.&#x0D; Cardiovasc. j. 2021; 13(2): 177-182

BackgroundPulmonary hypertension (PH) was recently recognized as a common complication of end-stage renal disease (ESRD) that causes an increased risk of mortality. Epidemiological data for this disorder in earlier stages of chronic kidney disease (CKD) and its association with cardiovascular (CV) morbidity are scarce.MethodsWe retrospectively analyzed 2,351 Chinese CKD patients with complete clinical records and echocardiography data between Jan 2008 and May 2012. The patients were divided into the following 6 groups: CKD Stages 1–4; Stage 5 for those not on or initiated on hemodialysis for <3 months; and Stage 5D for the patients undergoing hemodialysis for ≥3 months. The prevalence of PH and CV morbidity was investigated, and their association was evaluated with a logistic regression model.ResultsPH was detected in 426 patients (18.1%). Mild, moderate and severe PH was diagnosed in 12.1%, 4.9% and 1.1% of the patients, respectively. Severe PH was detected in CKD Stages 5 and 5D. CV morbidity was found in 645 patients (27.4%). Compared with the non-PH group, the PH group had a higher risk for cardiac disease but not for cerebrovascular disease risk. PH severity was associated with cardiac morbidity risk [odds ratio (95% CI) for mild PH: 1.79 (1.30–2.47); moderate PH: 2.75 (1.73–4.37); severe PH: 3.90 (1.46–10.42)].ConclusionsOur study showed for the first time the epidemiology profile of PH across the spectrum of CKD. Mild-to-moderate PH occurs with more frequency in advanced CKD, and severe PH is scarce in non-ESRD CKD. PH in CKD is associated with cardiac but not cerebrovascular disease, with increasing cardiac morbidity seen with increasing PH severity. Evidence from prospective studies addressing PH in this population is needed to predict cardiac events.

We aimed to assess the accuracy of Doppler tissue imaging (DTI) in detecting right ventricle (RV) dysfunction and electromechanical coupling alteration following pulmonary hypertension (PHT) in rat. PHT was induced by chronic hypoxia exposure (hypoxic PHT) or monocrotaline treatment (monocrotaline PHT). In both PHT models, we observed transparietal RV pressure increase and remodeling, including hypertrophy and dilation. Conventional echocardiography provided evidence for pulmonary outflow impairment with midsystolic notch and acceleration time decrease in PHT groups (21.7 +/- 1.6 and 13.2 +/- 2.9 ms in hypoxic and monocrotaline PHT groups vs. 28.1 +/- 1.0 ms in control). RV shortening fraction was decreased in the monocrotaline PHT group compared with the hypoxic PHT and control groups. Combining conventional Doppler and DTI was more helpful to detect RV diastolic dysfunction in the monocrotaline PHT group (E/Ea ratio = 17.0 +/- 1.4) compared with the hypoxic PHT and control groups (11.5 +/- 0.7 and 10.2 +/- 0.4, respectively). Tei index measured using DTI highlighted global RV dysfunction in the monocrotaline PHT group (1.36 +/- 0.24 vs. 0.92 +/- 0.05 and 0.86 +/- 0.05 in the hypoxic PHT and control groups, respectively). Q-Sm time measured from the onset of Q wave to the onset of DTI Sm wave was increased in both PHT groups. PHT-induced electromechanical coupling alteration was confirmed by in vitro activation-contraction delay measurements on isolated RV papillary muscle, and both Q-Sm time and activation-contraction delay were correlated with PHT severity. We demonstrated that Q-Sm time measured in DTI was an easily and convenient index to detect early RV electromechanical coupling alteration in both moderate and severe PHT.

Background and Aims:There is conflicting evidence on adverse effect of Pulmonary Arterial Hypertension (PAH) on outcomes after cardiac surgery for rheumatic heart disease (RHD). The authors studied Indian patients with RHD and preoperative PAH, who undergo cardiac surgery with a hypothesis that they have poor short and long-term outcomes.Methods:This was a retrospective observational study of 407 patients. The patients were divided in three groups based on PAH estimated on echocardiograph as; no or mild PAH (pulmonary artery systolic pressure (PASP) <30 mm of Hg); moderate PAH (PASP 31-55 mm of Hg) and severe PAH (PASP >55 mm of Hg). The primary endpoint was in-hospital mortality and major morbidities; while secondary endpoint was long-term survival.Results:In-hospital mortality was 24 (5.9%); and was not different in patients with severe, (9.1%), moderate (4.5%) or mild PAH (2.8%) (P = 0.09). Patients with severe PAH had higher incidence of prolonged ventilation (P = 0.007). Factors independently associated with mortality were; >2-packed cell transfusion, prolonged ventilation and acute kidney injury but not moderate and severe PAH. Patients with mitral stenosis (MS) and severe PAH had significantly higher mortality as compared to no or mild PAH (P = 0.03) on long-term follow-up [81.37% (mean duration 19.40 ± 14.10 months)], mortality was 8% and not statistically different (P = 0.25) across PAH categories.Conclusion:Moderate and severe PAH does not affect short and long term outcomes of patients undergoing valve surgery for RHD. Patients with MS with severe PAH had higher mortality compared to those with no PAH.

The Cardio-Obstetrics Patient and the Cardiothoracic Anesthesiologist

It is generally believed that pulmonary hypertension (PHT) adversely affects outcome after liver transplantation (LT). Most transplant units consider severe PHT to be an absolute contraindication to LT. We examined the outcome of 145 patients who underwent LT between 1997 and 1999. Pulmonary artery pressures (PAPs) had been measured before surgery. Pre-LT workup included electrocardiography and echocardiography for the majority of patients. Also, the liver unit database was screened for patients with known PHT who had undergone LT before 1997. Based on pulmonary flotation catheter measurements made after the induction of anesthesia for LT, PHT was defined as mild or moderate to severe if the mean PAP (MPAP) exceeded 25 and 35 mm Hg, respectively. The incidence of PHT was 26% (38 of 145 patients); 31 of 38 patients had mild PHT. Kaplan-Meier survival analysis did not show a significant survival benefit for patients with normal PAPs compared with patients with PHT (all, mild, moderate to severe). For surviving patients, the duration of ventilation and intensive care unit stay was unaffected by PHT. Four of 5 patients (identified from the database 1982 to 1999) with MPAPs greater than 40 mm Hg survived LT by more than 1 year. PHT of this severity was usually associated with specific and suggestive abnormality of the echocardiogram. Mild PHT is common and does not affect patient outcome after LT. Moderate and severe PHT are uncommon. Our analysis suggests that when the cardiac index is preserved, the majority of patients with moderate and severe PHT can survive LT, and they will not die of PHT during long-term follow-up. Echocardiography detects most severe PHT, but not mild and moderate PHT.

Objective To investigate the correlation between pulmonary artery systolic pressure and ET-1 and VEGF in patients with congenital heart disease before and after transcatheter closure. Method s 90 patients with right shunting CHD were divided into four groups according to the pulmonary artery systolic pressure (PASP): non pulmonary hypertension (PH) group (PASP <30 mmHg, 13 patients), mild PH group (30 mmHg ≤ PASP <50 mmHg, 24 patients), moderate PH group (50 mmHg ≤ PASP <70 mmHg, 31 patients), severe PH group (≥70 mmHg, 22 patients). The levels of ET-1 and VEGF were measured before operation, at one day after operation, one week after operation, and one month after operation, and the relationship between ET, VEGF, and PASP were analyzed. Result s Before operation, the levels of ET-1 and VEGF in mild PH group, moderate PH group, and severe PH group were significantly higher than those in non PH group (P<0.05), the levels of ET-1 and VEGF in moderate PH group and severe PH group were higher than those in mild PH group (P<0.05), the levels of ET-1 and VEGF in severe PH group were higher than those in moderate PH group (P<0.05). Linear correlation analysis showed that PASP was positively correlated with the level of plasma ET-1 before operation, at one day after operation, one week after operation, and one month after operation (r=0.713, 0.688, 0.686, 0.669, P<0.05), and serum VEGF (r=0.684, 0.700, 0.674, 0.645, P<0.05). There was a positive correlation between the level of ET-1 and VEGF in CHD patients before operation, at one day after operation, one week after operation, and one month after operation (r=0.525, 0.490, 0.491, 0.560, P<0.05). Conclusions Among CHD patients with left to right shunt, with the increase of pulmonary artery pressure, the levels of ET-1 and VEGF in the blood increase, which are positively correlated with PASP. After operation, we can evaluate the effect of transcatheter closure by detecting the levels of ET-1 and VEGF, and fully understand the roles of ET-1 and VEGF in the development of PH. The decrease of ET-1 and VEGF through intervention may be helpful to delay the progress of PH. Key words: Congenital heart disease; Pulmonary hypertension; Transcatheter closure; Endothelin-1; Vascular endothelial growth factor

Hypoxia causes pulmonary vasoconstriction. Regional hypoxic vasoconstriction improves the matching of perfusion to alveolar ventilation. Global hypoxic vasoconstriction increases right ventricular afterload. The hypoxic pulmonary pressor response is universal in mammals and in birds, but with considerable interspecies and interindividual variability. Chronic hypoxia induces pulmonary hypertension in proportion to initial vasoconstriction. Prolonged hypoxic exposure is also associated with an increase in red blood cell mass, which aggravates pulmonary hypertension by an increase in blood viscosity. Hypoxic pulmonary hypertension in humans is usually mild to moderate, but pulmonary vascular pressure-flow relationships are steep, which corresponds to a substantial afterload on the right ventricle during exercise. A partial recovery of 10-25% of the hypoxia-induced decrease in maximal oxygen uptake has been reported with intake-specific pulmonary vasodilating interventions. Hypoxia has been reported to decrease myocardial fibre contractility in vitro. However, the acutely hypoxic right ventricle remains able to preserve the coupling of its contractility to increased afterload in intact animals. Echocardiographic studies of the right ventricle in healthy hypoxic human subjects show altered diastolic function, but systolic function that is preserved or even increased acutely and slightly depressed chronically. These findings are more pronounced in patients with chronic mountain sickness. Their clinical significance remains incompletely understood. Almost no imaging studies of right ventricular function have been reported in a minority of subjects who develop severe pulmonary hypertension and clinical right ventricular failure in hypoxia. No imaging studies of right ventricular function during hypoxic exercise in normal subjects are yet available. Thus, while it is plausible that the right ventricle limits exercise capacity in hypoxia, this still needs to be firmly established.

BackgroundThe aim of this study was to evaluate the pregnancy feasibility of women with mild pulmonary hypertension according to pregnancy outcomes.MethodsThis systematic review and meta-analysis compared the differences in maternal and fetal outcomes between mild and moderate-to-severe pulmonary hypertension. Relevant English and Chinese literature were searched in the PubMed, Embase, Cochrane Central Register of Controlled Trials (COCHRANE), CNKI, WanFang Data, and VIP databases between January 1st, 1990 and April 18th, 2023, and the references of the included articles and relevant systematic reviews were reviewed to determine whether studies were missed. The inclusion criteria were randomized controlled and observational studies (including case-control studies and cohort studies) examining maternal and fetal pregnancy outcomes with pulmonary hypertension. Conference abstracts, case reports, case series reports, non-comparative studies, and review articles were excluded.ResultsThis meta-analysis included 32 studies. In this study, maternal and fetal outcomes were better in the mild pulmonary hypertension group than in the moderate-to-severe group. Regarding maternal mortality, the mild group was much lower than the moderate to severe group. We found a significant decrease in maternal mortality in the mild group after 2010. However, no significant difference in maternal mortality before and after 2010 was observed in the moderate to severe group. Cardiac complications, ICU admission, neonatal preterm birth, small for gestational age infants, low birth weight infants, neonatal asphyxia, and neonatal mortality were significantly lower in the mild pulmonary hypertension group than in the moderate to severe pulmonary hypertension group. The cesarean section rates of the two groups were similar. However, the vaginal delivery rate in the mild pulmonary hypertension group was significantly higher than that in the moderate to severe pulmonary hypertension group.ConclusionsThis meta-analysis confirmed that pregnancies with mild pulmonary hypertension had significantly better maternal and fetal outcomes than those with moderate to severe pulmonary hypertension. For patients with mild pulmonary hypertension and good cardiac function, continued pregnancy or even delivery should be considered under multidisciplinary monitoring. However, maternal and fetal complications with moderate to severe pulmonary hypertension significantly increase. Hence, it is essential to evaluate pregnancy risk and terminate it in time.

Pulmonary hypertension predicts adverse cardiac events after restrictive mitral annuloplasty for severe functional mitral regurgitation