A novel semi-automated method to improve estimation of right ventricular systolic pressure by Doppler ultrasound

Objective: Patients with heart failure (HF) and pulmonary hypertension (PH) have worse outcomes after cardiac resynchronization therapy (CRT). The relationship of circulating HF biomarkers and right ventricular systolic pressure (RVSP) may provide insight to the mechanism between PH and poor CRT response. Methods: In 90 patients (age 65 ± 13, 78% male, EF 26 ± 8%, RVSP 44 ± 12 mmHg) undergoing CRT, we measured baseline RVSP by echocardiography and obtained peripheral blood samples drawn at the time of device implantation. We measured levels of established and emerging HF biomarkers (Table 1). CRT non-response was defined as no improvement of adjudicated HF Clinical Composite Score at 6 months. Major adverse cardiac event (MACE) was defined as composite endpoint of death, cardiac transplant, left ventricular assist device, and HF hospitalization within 2 years. Results: There were 34% CRT non-responders and 27% had MACE. Per 1 unit increase in log-transformed RVSP, there was an 11-fold increase risk of having CRT non-response (odd ratio [OR] 11.0, p=0.01) and over 5-fold increase of developing 2-year MACE (hazard ratio [HR] 5.8, p=0.02). When comparing patients with severe PH (RVSP>60 mmHg) to those without PH (RVSP < 35 mmHg), there was an 8-fold increase in CRT nonresponse (OR 8.4, p=0.03) but no difference in MACE (p=NS). RVSP was correlated with increased biomarker levels of myocardial stretch and fibrosis, but not myocardial necrosis (Table 1). Conclusions: Higher RVSP is associated with greater rates of CRT non-response and adverse clinical outcomes. The mechanistic association between severe PH and CRT nonresponse may be explained by the biomarker profile reflective of myocardial wall stretch and fibrosis.

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Right ventricular pressure response to +GZ acceleration stress

Journal of Applied Physiology ◽

10.1152/jappl.1982.53.4.908 ◽

1982 ◽

Vol 53 (4) ◽

pp. 908-913 ◽

Cited By ~ 2

Author(s):

J. E. Whinnery ◽

M. H. Laughlin

Keyword(s):

Right Ventricular ◽

Diastolic Pressure ◽

Vena Cava ◽

Systolic Pressure ◽

Ventricular Pressure ◽

Miniature Swine ◽

Right Ventricular Systolic Pressure ◽

Ventricular Systolic Pressure ◽

The Right ◽

Acceleration Stress

Measurements of right ventricular pressure in miniature swine were made at +Gz levels from +1 through +9 Gz. Polyethylene catheters were chronically placed in the cranial vena cava of five 2-yr-old female miniature swine (35–50 kg). The catheters were large enough to allow the introduction of a Millar pressure transducer into the venous system for placement in the right heart. The animals were fitted with an abdominal anti-G suit, restrained in a fiberglass couch, and exposed to the various +Gz levels on a centrifuge while fully conscious and unanesthetized. Right ventricular pressure and heart rate were measured during and for 2 min following 30-s exposures to each level of +Gz stress. The maximum right ventricular systolic pressure observed during +Gz was 200 Torr at +5 Gz with the maximum diastolic pressure being 88 Torr observed at +5 Gz. Mean heart rates were 200–210 beats/min at all levels of +Gz greater than or equal to +3 Gz when the animal remained stable. Mean maximum right ventricular pressures during +Gz stress were observed to increase through +5 Gz (85 Torr) and to decrease at higher levels of +Gz, indicating that through +5 Gz there is at least a partial compensation during acceleration stress. Decompensation in response to the stress began to occur during acceleration above +5 Gz with all animals decompensating during +9 Gz.

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Theoretical validity of predicting right ventricular systolic pressure by a quantitative index of interventricular septal displacement in acute right ventricular pressure overload.

Japanese Circulation Journal ◽

10.1253/jcj.55.238 ◽

1991 ◽

Vol 55 (3) ◽

pp. 238-249 ◽

Cited By ~ 2

Author(s):

SATOSHI TANAZAWA ◽

TETSURO IMAMOTO ◽

HIROHISA YAMASHITA

Keyword(s):

Right Ventricular ◽

Systolic Pressure ◽

Pressure Overload ◽

Ventricular Pressure ◽

Quantitative Index ◽

Right Ventricular Systolic Pressure ◽

Ventricular Systolic Pressure

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The effect of endogenous estrogen on Doppler-estimated right ventricular systolic pressure during exercise

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y2012-100 ◽

2012 ◽

Vol 90 (10) ◽

pp. 1364-1371

Author(s):

Vicki N. Wang ◽

Mavra Ahmed ◽

Amelia Ciofani ◽

Zion Sasson ◽

John T. Granton ◽

...

Keyword(s):

Blood Pressure ◽

Menstrual Cycle ◽

Right Ventricular ◽

Systolic Pressure ◽

Rate Pressure Product ◽

Right Ventricular Systolic Pressure ◽

Ventricular Systolic Pressure ◽

Early Exercise ◽

Endogenous Estrogen ◽

Response To Exercise

We evaluated the effect of endogenous estrogen levels on exercise-related changes in right ventricular systolic pressure (RVSP) of healthy, eumenorrheic, sedentary women. Volunteers were studied at two separates phases of the menstrual cycle (LO and HI estrogen phases), exercised on a semi-supine ergometer with escalating workload and monitored continuously by 12-lead ECG and automated blood pressure cuff. At each exercise stage, Doppler echocardiography measurements were obtained and analyzed to determine RVSP. Fourteen subjects (age 24 ± 5) were studied. Exercise duration was significantly higher on the HI estrogen day, but no significant differences in hemodynamic response to exercise were found between the two study days. There were also no significant differences with respect to heart rate (HR) acceleration during early exercise, as well as resting and peak RVSP, HR, blood pressure, and rate pressure product. Doppler-estimated RVSP demonstrated a linear relationship to HR at a ratio of 1 mm Hg (1 mm Hg = 133.3224 Pa) for every 5 bpm (beats per minute) increase in HR. There were no differences in the slope of this relationship between HI and LO estrogen phases of the menstrual cycle. Our findings did not demonstrate any effect of endogenous estrogen levels on the modulation of the pulmonary vascular response to exercise in healthy women.

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Echocardiographic Pulmonary to Left Atrial Ratio (ePLAR): A Comparison Study between Ironman Athletes, Age Matched Controls and A General Community Cohort

Journal of Clinical Medicine ◽

10.3390/jcm8101756 ◽

2019 ◽

Vol 8 (10) ◽

pp. 1756 ◽

Cited By ~ 1

Author(s):

Tran ◽

Kwon ◽

Holt ◽

Kierle ◽

Fitzgerald ◽

...

Keyword(s):

Right Ventricular ◽

Pulmonary Vascular Resistance ◽

Vascular Resistance ◽

Left Atrial ◽

Systolic Pressure ◽

Exercise Stress ◽

Control Group ◽

Right Ventricular Systolic Pressure ◽

Ventricular Systolic Pressure ◽

General Community

Background: During exercise there is a proportionally lower rise in systemic and pulmonary pressures compared to cardiac output due to reduced vascular resistance. Invasive exercise data suggest that systemic vascular resistance reduces more than pulmonary vascular resistance. The aim of this study was the non-invasive assessment of exercise hemodynamics in ironman athletes, compared with an age matched control group and a larger general community cohort. Methods: 20 ironman athletes (40 ± 11 years, 17 male) were compared with 20 age matched non-athlete controls (43 ± 7 years, 10 male) and a general community cohort of 230 non-athletes individuals (66 ± 11 years, 155 male), at rest and after maximal-symptom limited treadmill exercise stress echocardiography. Left heart parameters (mitral E-wave, e’-wave and E/e’) and right heart parameters (tricuspid regurgitation maximum velocity and right ventricular systolic pressure), were used to calculate the echocardiographic Pulmonary to Left Atrial Ratio (ePLAR) value of the three groups. Results: Athletes exercised for 12.2 ± 0.53 minutes, age matched controls for 10.1 ± 2.8 minutes and general community cohort for 8.3 ± 2.6 minutes. Mitral E/e’ rose slightly for athletes (0.9 ± 1.8), age matched controls (0.6 ± 3.0) and non-athletes (0.4 ± 3.2). Right ventricular systolic pressure increased significantly more in athletes than in both non-athlete cohorts (35.6 ± 17 mmHg vs. 20.4±10.8mmHg and 18 ± 9.6 mmHg). The marker of trans-pulmonary gradient, ePLAR, rose significantly more in athletes than in both non-athlete groups (0.15 ± 0.1 m/s vs. 0.07 ± 0.1 m/s). Conclusions: Pulmonary pressures increased proportionally four-fold compared with systemic pressures in ironman athletes. This increase in pulmonary vascular resistance corresponded with a two-fold increase in ePLAR. These changes were exaggerated compared with both non-ironman cohorts. Such changes have been previously suggested to lead to right ventricle dysfunction, arrhythmias and sudden cardiac death.

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Chronic Hypoxia Decreases Endothelial Connexin 40, Attenuates Endothelium‐Dependent Hyperpolarization–Mediated Relaxation in Small Distal Pulmonary Arteries, and Leads to Pulmonary Hypertension

Journal of the American Heart Association ◽

10.1161/jaha.120.018327 ◽

2020 ◽

Vol 9 (24) ◽

Author(s):

Rui Si ◽

Qian Zhang ◽

Jody Tori O. Cabrera ◽

Qiuyu Zheng ◽

Atsumi Tsuji‐Hosokawa ◽

...

Keyword(s):

Endothelial Cells ◽

Pulmonary Hypertension ◽

Right Ventricular ◽

Knockout Mice ◽

Chronic Hypoxia ◽

Systolic Pressure ◽

Right Ventricular Systolic Pressure ◽

Ventricular Systolic Pressure ◽

Pulmonary Endothelial Cells ◽

Endothelium Dependent Relaxation

Background Abnormal endothelial function in the lungs is implicated in the development of pulmonary hypertension; however, there is little information about the difference of endothelial function between small distal pulmonary artery (PA) and large proximal PA and their contribution to the development of pulmonary hypertension. Herein, we investigate endothelium‐dependent relaxation in different orders of PAs and examine the molecular mechanisms by which chronic hypoxia attenuates endothelium‐dependent pulmonary vasodilation, leading to pulmonary hypertension. Methods and Results Endothelium‐dependent relaxation in large proximal PAs (second order) was primarily caused by releasing NO from the endothelium, whereas endothelium‐dependent hyperpolarization (EDH)–mediated vasodilation was prominent in small distal PAs (fourth–fifth order). Chronic hypoxia abolished EDH‐mediated relaxation in small distal PAs without affecting smooth muscle–dependent relaxation. RNA‐sequencing data revealed that, among genes related to EDH, the levels of Cx37 , Cx40 , Cx43 , and IK were altered in mouse pulmonary endothelial cells isolated from chronically hypoxic mice in comparison to mouse pulmonary endothelial cells from normoxic control mice. The protein levels were significantly lower for connexin 40 (Cx40) and higher for connexin 37 in mouse pulmonary endothelial cells from hypoxic mice than normoxic mice. Cx40 knockout mice exhibited significant attenuation of EDH‐mediated relaxation and marked increase in right ventricular systolic pressure. Interestingly, chronic hypoxia led to a further increase in right ventricular systolic pressure in Cx40 knockout mice without altering EDH‐mediated relaxation. Furthermore, overexpression of Cx40 significantly decreased right ventricular systolic pressure in chronically hypoxic mice. Conclusions These data suggest that chronic hypoxia‐induced downregulation of endothelial Cx40 results in impaired EDH‐mediated relaxation in small distal PAs and contributes to the development of pulmonary hypertension.

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