Abstract 13973: Impaired Right Ventricular Hemodynamics Suggest Preclinical Pulmonary Hypertension in Patients With Metabolic Syndrome

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Deepa M Gopal ◽  
Yi-Chih Wang ◽  
Nir Ayalon ◽  
Courtney Donohue ◽  
Rajalakshmi Santhanakrishnan ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Doppler Measurement ◽  
Ejection Time ◽  
Pulsed Wave Doppler ◽  
Lv Diastolic Dysfunction

Introduction: Metabolic syndrome (MetS) is associated with preclinical metabolic heart disease (MHD) as reflected by left ventricular (LV) diastolic dysfunction. Very little is known about right ventricular (RV) function and/or pulmonary hypertension in MetS or early MHD. Hypothesis: We tested the hypothesis that that MetS is associated with subclinical RV dysfunction and pulmonary hypertension. Methods: A total of 164 subjects with MetS but without cardiovascular disease (mean age 45 years, 71% women, mean BMI 41 kg/m 2 ), 40 similarly obese controls without MetS, and 36 non-obese healthy controls underwent echocardiography, including pulsed-wave Doppler measurement of pulmonary artery acceleration time (PAAT) and ejection time (ET). PA systolic pressure was estimated from PAAT using validated equations. Results: MetS was associated with lower tricuspid valve e', shorter PAAT, shorter ET, and larger PA diameter compared with controls (Table). A total of 24% of individuals with MetS had an abnormal PAAT (<100 msec). Estimated PA systolic pressure based on PAAT was 42±10 mmHg in MetS compared with 32±10 and 32±9 mmHg in healthy and obese controls (P for ANOVA <0.0001). In contrast, RV structure and systolic function were similar in MetS compared with controls ( Table ). After adjustment for age, sex, hypertension, diabetes, and body-mass index, MetS remained associated with shorter PAAT (P=0.03 vs healthy; P=0.0005 vs obese). Among MetS, PAAT was correlated with mitral mean e’ (r=0.20, P=0.004), E/A ratio (r=0.21, P=0.008), and tricuspid e’ (r=0.20, P=0.04). A total of 40% of participants with abnormal PAAT also had low mean e’ (<8 cm/s). Conclusions: MetS is associated with abnormal RV hemodynamics as evidenced by shorter PAAT, which correlates with measures of LV diastolic function. Estimated PA systolic pressures are significantly higher in preclinical MetS and MHD, and raise the possibility that pulmonary hypertension contributes to the pathophysiology of MHD.

scholarly journals Apelin decreases myocardial injury and improves right ventricular function in monocrotaline-induced pulmonary hypertension

2009 ◽  
Vol 296 (6) ◽  
pp. H2007-H2014 ◽  
Author(s):  
Inês Falcão-Pires ◽  
Nádia Gonçalves ◽  
Tiago Henriques-Coelho ◽  
Daniel Moreira-Gonçalves ◽  
Roberto Roncon-Albuquerque ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Chronic Administration ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Peak Rate ◽  
Male Wistar Rats ◽  
Neurohumoral Activation

We investigated the endogenous production of apelin and the cardiac and pulmonary effects of its chronic administration in monocrotaline (MCT)-induced pulmonary hypertension (PH). Male Wistar rats were injected with MCT (60 mg/kg sc) or vehicle ( day 0). One week later, these animals were randomly treated during 17 days with pyroglutamylated apelin-13 (Pyr-AP13; 200 μg·kg−1·day−1 ip) or a similar volume of saline, resulting in four groups: sham ( n = 11), sham-AP ( n = 11), MCT ( n = 16), and MCT-AP ( n = 13). On day 25, right ventricular (RV) and left ventricular (LV) hemodynamic and morphometric parameters were assessed. Tissue and plasma samples were collected for histological and molecular analysis. When compared with sham, the MCT group presented a significant increase of RV mass (166 ± 38%), diameter of cardiomyocyte (40 ± 10%), myocardial fibrosis (95 ± 20%), peak systolic pressure (99 ± 22%), peak rate of ventricular pressure rise (dP/d tmax; 74 ± 24%), peak rate of ventricular pressure decline (dP/d tmin; 73 ± 19%), and time constant τ (55 ± 16%). In these animals, RV expression of apelin (−73 ± 10%) and its receptor APJ (−61 ± 20%) was downregulated, whereas mRNA expression of type B natriuretic peptide (9,606 ± 713%), angiotensinogen (191 ± 147%), endothelin-1 (RV, 497 ± 156%; and LV, 799 ± 309%), plasmatic levels of apelin (104 ± 48%), and angiotensin 1-7 (161 ± 151%) were increased. Chronic treatment with Pyr-AP13 significantly attenuated or normalized these changes, preventing apelin-APJ mRNA downregulation and PH-induced neurohumoral activation of several vasoconstrictors, which exacerbates apelin-APJ vasodilator effects. Therefore, apelin delayed the progression of RV hypertrophy and diastolic dysfunction. Together, these observations suggest that the apelin-APJ system may play an important role in the pathophysiology of PH, representing a potential therapeutic target since it significantly attenuates RV overload and PH-induced neurohumoral activation.

Pulmonary Venous Hypertension: A Pulmonologist's Perspective

2011 ◽  
Vol 10 (1) ◽  
pp. 18-23 ◽  
Author(s):  
Francisco Soto
Keyword(s):  
Pulmonary Hypertension ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Venous Hypertension ◽  
Systemic Hypertension ◽  
Pulmonary Artery Systolic Pressure ◽  
Obstructive Sleep ◽  
Group 2 ◽  
Group 1

Increased pulmonary hypertension (PH) awareness in the general public and among health providers has led to an increase in referral of patients who are found to have elevated estimates of pulmonary artery systolic pressure (PASP) on a transthoracic echocardiogram (TTE), without other strong features suggestive of precapillary PH (pulmonary arterial hypertension; PAH). Some of these patients undergo TTE as part of their workup for unexplained dyspnea that appears out of proportion to their other comorbidities. Many of these patients are older individuals with underlying conditions such as systemic hypertension (HTN), diabetes mellitus (DM), coronary artery disease (CAD), and obstructive sleep apnea (OSA). While some of them may have PAH, accumulated experience in the PH community suggests that many of these patients will be ultimately found to have elevated left ventricular (LV) filling pressures and impaired LV relaxation as the cause of their dyspnea and elevation of pulmonary pressures on TTE.12 These findings are consistent with a form of Group 2 PH termed LV diastolic dysfunction, more recently termed heart failure with preserved left ventricular systolic function (HFpEF) (Table 1).2 Other forms of Group 2 PH, defined as “pulmonary hypertension owing to left-sided heart disease,” include LV systolic dysfunction or left-sided valvular disease.2 For the purpose of this article, the term pulmonary venous hypertension (PVH) will be used to refer to Group 2 PH, HFpEF. Being able to accurately discriminate PAH (precapillary; Group 1 PH) from PVH (postcapillary; Group 2 PH) is critical to determine and apply the appropriate treatment course. This is a difficult, yet frequently encountered clinical dilemma, which can fall into a “gray zone” with respect to clinical classification. We will provide important clinical features that should heighten the clinician's awareness and suspicion of this rapidly growing phenomenon. These features are critical when trying to differentiate PAH (Group 1 PH) from PVH (Group 2 PH).

Abstract 4389: Right Ventricular Diastolic Function in Pulmonary Hypertension

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Angel Lopez-Candales ◽  
Ananth Eleswarapu ◽  
Kathy Edelman
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricular ◽  
Diastolic Dysfunction ◽  
Systolic Function ◽  
Left Ventricular ◽  
Diastolic Flow ◽  
Group I ◽  
Diastolic Interval ◽  
Ventricular Diastolic Dysfunction ◽  
Group Ii

Background : Left ventricular diastolic dysfunction is associated with worse outcomes in patients with severe chronic elevation in pulmonary artery systolic pressures (PASP); however, little is known if right ventricular diastolic dysfunction (RVDD) is also present in these patients. Methods : Color M-mode to measure RV propagation velocity (Vp) and tissue Doppler imaging (TDI) of the tricuspid valve annulus (TVa) were done in 21 patients (Group I: mean age 54 ± 15, mean PASP 80 ± 31 mmHg) and in 19 healthy individuals (Group II: mean age 51 ± 14 years, PASP 30 ± 7 mmHg). All subjects were in normal sinus rhythm and normal left ventricular systolic function. Results : Despite elevation in PASP, Group I RV systolic function measured by both TVa excursion (2.01 ± 0.7 cm) and TVa systolic velocity (0.10 ± 0.04 cm/s) were no different than Group II (2.5 ± 0.5 cm and 0.12 ± 0.03 cm/s, respectively). Even though there was no difference in either early (0.11 ± 0.04 versus 0.13 ± 0.04 cm/s) versus late (0.15 ± 0.05 versus 0.13 ± 0.04 cm/s) diastolic velocities by TDI; a lower Vp was seen in Group I (28 ± 12 cm/s) than Group II (41 ± 15 cm/s, p < 0.01) with a significantly shorter diastolic interval (259 ± 90 versus 390 ± 80 ms, p < 0.0001). Representative color M-mode images are shown in the Figure . Conclusions : Routine use of TVA TDI appears to be less useful than color M-mode to appreciate RV diastole as it shows a slower Vp with flows shifted later in diastole. In addition, these patients also demonstrate a shorter diastolic interval. Further studies are now required to prospectively assess the effects of pulmonary hypertension in clinical outcomes in patients manifesting RVDD. Figure. (A) Color M-mode image of a patient artery systolic pressures demonstrating predominantly early diastolic flow. (B) Color M-mode image from a patient with pulmonary hypertension showing predominantly late diastolic flow.

scholarly journals Tofogliflozin improved pulmonary hypertension due to heart failure with preserved ejection fraction in mice

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
Y J Joki ◽  
H K Konishi ◽  
K T Takasu ◽  
T M Minamino
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Right Ventricular ◽  
Heart Diseases ◽  
Sglt2 Inhibitor ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Chow Diet ◽  
Normal Chow

Abstract Introduction Pulmonary hypertension (PH) caused by left heart diseases is categorized as the group 2 (PH-LHD). PH-LHD due to heart failure with preserved LV ejection fraction (HFpEF) is more prevalent in patients with metabolic syndrome and shows poorer prognosis than LHD without PH. Tofogliflozin (TOFO) is an SGLT2 inhibitor utilized for diabetic treatment. Recent studies revealed that the SGLT2 inhibitor has a beneficial effect on heart failure; however, it remains unclear whether the SGLT2 inhibitor is effective for the treatment of PH-LHD. Hypothesis We hypothesized that TOFO has a protective effect on PH with HFpEF. Methods We generated two murine models for PH-LHD due to HFpEF, a transverse aortic constriction (TAC) model and a high fat diet (HFD) model. C57BL/6J mice were subjected to TAC and treated with TOFO (3 mg/kg) for 4weeks. In another model, AKR/J mice were fed HFD or normal chow diet and treated with TOFO (3mg/kg in water) for 20 weeks. We then measured physical data including body weight (BW), left ventricular weight (LV), right ventricular weight (RV), and right ventricular systolic pressure (RVSP) and performed echocardiography. Results Mice treated with TOFO demonstrated increased urine glucose level. TAC induced left ventricular hypertrophy and increased RVSP. TOFO treatment improved RV/LV ratio and RVSP in TAC mice (Figure 1). HFD fed AKR/J mice demonstrated increased BW and PH as demonstrated by increased RV/LV ratio and RVSP compared with the normal chow group. TOFO treatment ameliorated the increases of BW, RV/LV ratio, and RVSP in HFD fed AKR/J mice (Figure 2). Conclusions TOFO treatment improved pulmonary hypertension in two models for PH-LHD due to HFpEF, suggesting that the SGLT2 inhibitor is effective for the treatment of this condition. FUNDunding Acknowledgement Type of funding sources: None. Figure 2. TOFO reduced RVSP caused by HFD

scholarly journals Angiotensin-II type 1 receptor mediates pulmonary hypertension and right ventricular remodeling induced by inhaled nicotine.

2021 ◽  
Author(s):  
Nicholas D. Fried ◽  
Tamara M. Morris ◽  
Anna Whitehead ◽  
Eric Lazartigues ◽  
Xinping Yue ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Angiotensin Ii ◽  
Right Ventricular ◽  
Ventricular Remodeling ◽  
Electronic Cigarettes ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Internal Diameter ◽  
Serum Cotinine

Use of electronic cigarettes is rapidly increasing among youth and young adults, but little is known regarding the long-term cardiopulmonary health impacts of these nicotine-containing devices. Our group has previously demonstrated that chronic, inhaled nicotine induces pulmonary hypertension (PH) and right ventricular (RV) remodeling in mice. These changes were associated with upregulated RV angiotensin-converting enzyme (ACE). Angiotensin-II receptor blockers (ARBs) have been shown to reverse cigarette smoking-induced PH in rats. ACE inhibitor and ARB use in a large retrospective PH patient cohort is associated with improved survival. Here, we utilized losartan (an ARB specific for angiotensin-II type 1 receptor) to further explore nicotine-induced PH. Male C57BL/6 mice received nicotine vapor for 12 hours per day, and exposure was assessed using serum cotinine to achieve levels comparable to human smokers or electronic cigarette users. Mice were exposed to nicotine for 8 weeks and a subset was treated with losartan via osmotic minipump. Cardiac function was assessed using echocardiography and catheterization. Although nicotine exposure increased angiotensin-II in the RV and lung, this finding was non-significant. Chronic, inhaled nicotine significantly increased RV systolic pressure and RV free wall thickness versus air control. These parameters were significantly lower in mice receiving both nicotine and losartan. Nicotine significantly increased RV internal diameter, with no differences seen between the nicotine and nicotine-losartan group. Neither nicotine nor losartan effect left ventricular structure or function. These findings provide the first evidence that antagonism of the angiotensin-II type 1 receptor can ameliorate chronic, inhaled nicotine-induced PH and RV remodeling.

Prospective Assessment of Pulmonary Hypertension in Children with Chuvash Polycythemia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3665-3665
Author(s):  
Niti Dham ◽  
Craig Sable ◽  
Daniel Okhotin ◽  
Adelina Sergueeva ◽  
Galina Miasnikova ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Diastolic Function ◽  
Varicose Veins ◽  
Systolic Function ◽  
Pressure Ratio ◽  
Systolic Pressure ◽  
Autosomal Recessive Disorder ◽  
Left Ventricular ◽  
Negative Regulator ◽  
Vascular Events

Abstract Background: Chuvash Polycythemia (CP) is an autosomal recessive disorder that is endemic to the Chuvash region of Russia; however, it does occur worldwide. It is characterized by a mutation (598C&gt;T) of the von Hippel Lindau gene, a negative regulator of hypoxia-sensing, and increased levels of hypoxia inducible factor-alpha during normoxia. CP is manifested by vertebral hemangiomas, varicose veins, hypotension, elevated concentrations of products of hypoxia-induced genes (serum vascular endothelial growth factor and endothelin-1), and premature mortality related to cerebral vascular events and peripheral thrombosis. Echocardiography (echo) studies in adults with CP suggest an increased prevalence of pulmonary hypertension (PH), but these findings have not been validated in children with CP. Methods: This work is supported by an NIH grant evaluating the prevalence, outcomes, pathophysiology, vascular response, and gene polymorphisms of PH in sickle cell disease and CP. We traveled to Cheboksary, Russia to prospectively enroll children with CP and age and gender matched controls to undergo echo for assessment of left ventricular (LV) systolic and diastolic function, LV size and mass, estimated right ventricular (RV) systolic pressure by tricuspid regurgitation velocity (TRV), and the RV to systemic systolic blood pressure (SBP) ratio. Data was compared between CP and control children. Results: 24 CP and 11 control patients were enrolled in the study. 20 CP and 9 control patients had measurable TRV. 4 of 20 CP and none of the control patients had TRV &gt; 2.5 m/sec (max TRV 2.89 m/sec). There was a trend towards higher TRV and estimated RV pressure in CP patients. Systolic function, LV size, and mass were the same in both groups. Diastolic function was normal in both groups but significantly better in CP patients. SBP was the same in both groups. Systemic mean and diastolic BP, adjusted for age, was significantly lower in CP children. Conclusions: Preliminary prospective data show a trend towards higher echo derived estimates of RV pressure in children with CP that can not be explained by hypertension or diastolic dysfunction. Rather, congenital upregulation of the hypoxic response may be responsible. Continued patient recruitment and correlation of TRV with other variables will allow for a better understanding of PH in children with CP. ECHO PARAMETERS CP Controls p TRV (m/sec) 2.24 ± 0.32 2.08 ± 0.14 0.08 RV systolic pressure (mm Hg) 25.4 ± 5.7 22.4 ± 2.4 0.06 RV/systemic pressure ratio 0.26 ± 0.06 0.24 ± 0.03 0.17 LV diastolic dimension z score 0.11 ± 0.91 −0.13 ± 0.79 0.42 LV Mass Index: g/m^2.7 25.8 ± 8.2 24.7 ± 6.5 0.68 Ejection fraction (%) 64.9 ± 3.7 64.7 ± 3.2 0.91 Mitral E/Tissue Doppler E 5.35 ± 0.81 6.48 ± 1.31 0.02

Abstract 16307: Tofogliflozin Improves Pulmonary Hypertension With Heart Failure With Preserved Ejection Fraction Mice

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Yusuke Joki ◽  
Hakuoh Konishi ◽  
Kiyoshi Takasu ◽  
Tohru Minamino
Keyword(s):  
Heart Failure ◽  
Pulmonary Hypertension ◽  
Ejection Fraction ◽  
Beneficial Effect ◽  
Right Ventricular ◽  
Sglt2 Inhibitor ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Sglt2 Inhibitors ◽  
Urine Glucose

Introduction: Pulmonary hypertension (PH) is a syndrome of increased pulmonary artery pressure and often leads to death. Left heart diseases(LHD) are frequently complicated by PH (PH-LHD), classified group2. In particular, PH with heart failure with preserved LV ejection fraction (HFpEF) is higher prevalence metabolic syndrome and poor prognosis than LHD without PH. Tofogliflozin (TOFO) is SGLT2 inhibitor as a therapeutic agent for diabetes. Recent study revealed SGLT2 inhibitors have a beneficial effect on heart failure. However it has not been clarified that SGLT2 inhibitors affect PH-LHD. This study examined whether TOFO improved for PH-LHD. Hypothesis: We hypothesis TOFO has a protective effect for PH with HFpEF. Methods: We used two HFpEF mice models, induced by transverse aortic constriction (TAC) surgery and high fat diet (HFD). TAC model: C57BL/6J mice were subjected to TAC. Sham and TAC mice were treated with TOFO 3mg/kg in water by day or only water. After 4weeks, each mouse was measured physical data, Body weight (BW), Left ventricular weight (LV), Right ventricular weight (RV), right ventricular systolic pressure (RVSP), UCG, collected blood and urine glucose. HFD model: AKR/J mice fed a HFD for 20weeks. Regular diet and HFD mice were treated with TOHO 3mg/kg in water by day or only water. 20weeks later each mouse measured above data. Results and Conclusions: Mice treated with TOFO had significantly higher urine glucose concentrations. TAC induced left ventricular hypertrophy, increased HW/BW ratio and RVSP. However TAC+TOFO mice were reduced hypertrophy and LV/BW ratio than TAC group. Moreover TAC+TOFO mice were improved RV/LV ratio and RVSP (Figure). AKR/J+HFD groups substantially higher BW and occurred PH than RFD groups. In contrast with HFD, TOFO treated group ameliorated BW, RW/LW ratio, moreover normal RVSP. These results showed Tofogliflozin had a beneficial effect for PH with HFpEF.

Left ventricular diastolic dysfunction and diseases severity contribute to impaired exercise capacity in systemic lupus erythematosus

Lupus ◽  
2021 ◽  
pp. 096120332110069
Author(s):  
Michał Ciurzyński ◽  
Anna Chrzanowska ◽  
Piotr Bienias ◽  
Justyna Domienik-Karłowicz ◽  
Piotr Sobieraj ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Right Ventricular ◽  
Diastolic Dysfunction ◽  
Exercise Capacity ◽  
Lupus Erythematosus ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Systemic Lupus ◽  
6Mwt Distance ◽  
Lv Diastolic Dysfunction

Objectives Patients with systemic lupus erythematosus (SLE) have a higher risk of myocardial involvement, which can result in ventricular dysfunction. The aim of our study was to estimate potential relationship between exercise capacity assessed by six minute walk test (6MWT) and echocardiographic parameters of left and right ventricular function in SLE patients. Methods We prospectively studied 66 SLE patients (57 F, age 44 (20–75) years) and 27 age matched healthy subjects. In addition to routine evaluation, 6MWT and transthoracic echocardiography including LV diastolic dysfunction parameters (E/A, E/É) were performed. Results While E/A was similar in both groups, E/E’ was higher in patients with SLE than in controls, 7.5 (4–22) vs 6.8 (1.6–9.4), p = 0.018. The mean 6MWT distance was significantly shorter in SLE (561.6 ± 150.7 vs 682.6 ± 98.1 m, p < 0.002). Among SLE patients only 53 (80.3%) were capable to walk at least 450 m, while in controls 27 (100%) (p = 0.013). We observed significant correlations between 6MWT distance and SLICC/ACR-DI (rho=−0.44, p < 0.001), E/A (rho = 0.30, p = 0.004), E/E’ (rho=−0.36, p < 0.001) in SLE patients. Univariable logistic regression models revealed that SLICC/ACR-DI, E/E’, tricuspid regurgitant peak gradient (TRPG), and right ventricular systolic pressure (RVSP) were associated with 6MWT distance lower than < 450 m. ROC curves shown high predictive value of E/E’ ratio, TRPG, RVSP in the prediction for 6MWT distance < 450 m. Conclusion Impaired exercise tolerance seems to result mainly from the severity of SLE and LV diastolic dysfunction.

Sign in / Sign up

Export Citation Format

Share Document