Interventricular Mechanical Asynchrony Due To Right Ventricular Pressure Overload in Pulmonary Hypertension Plays an Important Role in Impaired Left Ventricular Filling

Vonk‐Noordegraaf, Anton; Marcus, J. Tim; Gan, C. Tji-Joong; Boonstra, Anco; Postmus, Pieter E.

doi:10.1378/chest.128.6_suppl.628s

Cited by 47 publications

(34 citation statements)

References 5 publications

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“…A ratio of systolic to diastolic duration <1.00 was associated with low or no risk, a ratio 1.00 to 1.40 was associated with a moderate risk, and a ratio >1.40 was associated with a high risk of experiencing death or lung transplantation. 78 RV hypertension, dilation, and septal displacement also create RV dyssynchronous motion [81][82][83] and dyssynchronous RV-LV contraction. 65,83,84 Delayed RV lateral wall contraction and interventricular dyssynchrony in PAH are not related to QRS duration or abnormal electric activation such as that which occurs in left bundle-branch block but rather to RV wall stress, septal shift, LV end-diastolic volume, and stroke volume.…”

Section: Rv Versus LV Failure 1039mentioning

confidence: 99%

“…78 RV hypertension, dilation, and septal displacement also create RV dyssynchronous motion [81][82][83] and dyssynchronous RV-LV contraction. 65,83,84 Delayed RV lateral wall contraction and interventricular dyssynchrony in PAH are not related to QRS duration or abnormal electric activation such as that which occurs in left bundle-branch block but rather to RV wall stress, septal shift, LV end-diastolic volume, and stroke volume. 65,84 These ventricular-ventricular interactions almost certainly increase the ratio of systolic to diastolic duration because interventricular dyssynchrony is related to lengthening of the RV contraction.…”

Section: Rv Versus LV Failure 1039mentioning

confidence: 99%

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Right Versus Left Ventricular Failure

2014

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1033V entricular failure manifests in many forms, its underlying physiology ranging from overt left ventricular (LV) systolic dysfunction to isolated right ventricular (RV) diastolic dysfunction, and the wide portfolio of resulting symptoms vary from chronic fluid retention to acute multiorgan dysfunction and death. In this review, we discuss the morphological, functional, and molecular similarities and differences in RV and LV responses to adverse loading and failure. We further discuss whether LV and RV function and failure can truly be discussed as separate entities and thereby examine interactions between the ventricles that on one hand contribute to ventricular dysfunction but on the other may be harnessed for therapeutic benefit. Embryological and Physiological Differences Between the RV and LVThe RV and LV have different embryological origins.1 The LV originates from the primary heart field; the RV, from the secondary heart field. Consequently, several genes specifically control RV formation, including, among others, Hand2 and Tbx20.2 During gestation, the RV functions as the systemic ventricle ( Figure 1A). During fetal life, in addition to supplying the modest amount of pulmonary blood flow, the RV pumps blood to the lower body and placenta and contributes more than half of the combined cardiac output.3 With the transition from fetal to postnatal physiology and with the reduction in pulmonary vascular resistance, the subpulmonary RV transforms its morphology and geometry, becoming a thin-walled chamber to adopt its postnatal physiological characteristics. 4 Because it faces a low impedance pulmonary circulation, the normal postnatal RV maintains a cardiac output equal to that of the LV at approximately a fifth of the energy cost. The trapezoidal RV pressure-volume loop reflects this difference, with few if any isovolumic periods. Consequently, RV output starts early during pressure generation and is later maintained by a "hangout period" when antegrade flow continues into the pulmonary artery despite the onset of RV relaxation.5 In contrast, the rectangular LV pressure-volume loops reflect the LV square-wave pump function with distinct and well-developed isovolumic contraction and relaxation periods.6 Likewise, RV myocytes display faster twitch velocities than LV myocytes. 7The physiological differences are reflected in morphological differences between the ventricles (Table 1). The low-pressure RV is triangular in the sagittal plane and crescent-shaped in cross section as a result of the concave RV free wall and convex interventricular septum wrapping around the high-pressured, thick-walled, bullet-shaped LV. Consequently, although the normal RV has a lower ratio of volume to surface area and a thinner wall than the LV, 8 the low cavity pressure determines a lower wall stress and lower oxygen demands.Anatomic differences are also apparent in myocardial architecture. LV subepicardial and subendocardial fibers are oblique and helical with fiber angles ranging from 30° to 80° with a mean of ≈60°, whereas ...

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Section: Rv Versus LV Failure 1039mentioning

confidence: 99%

Section: Rv Versus LV Failure 1039mentioning

confidence: 99%

Right Versus Left Ventricular Failure

2014

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“…Tagged MRI study indicates that this paradoxical septal motion is a result of higher pressure in the right than in the left ventricle leading to interventricular asynchrony due to a prolonged right ventricle contraction. This ventricular asynchrony impedes left ventricle diastolic filling, causing a lowered LVEDV [112,113]. Right intraventricular dyssynchrony is also more prevalent in patients with PAH compared with controls as measured by two-dimensional strain echocardiography [114] and Doppler echocardiography [115].…”

Section: Future Directionsmentioning

confidence: 99%

The value of tools to assess pulmonary arterial hypertension

Gupta¹,

Ghimire²,

Naeije³

2011

European Respiratory Review

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Pulmonary hypertension is a common but complex clinical problem. When suspected in an appropriate clinical setting or detected incidetally, an array of investigative tools are employed with an intent to confirm the diagnosis, define aetiology, evaluate the functional and haemodynamic impairment, define treatment options, monitor the therapy, and establish long-term prognosis. However, no single tool provides comprehensive information that encompasses the aforementioned aims. Therefore, judicious use of these tools is of paramount importance, in order to maximise outcome and cost-effectiveness, while minimising risks and redundancies. Furthermore, a number of promising tools and techniques are emerging rapidly in the arena of pulmonary hypertension. These tools augment our understanding of pathophysiology and natural history of pulmonary hypertension. There is, therefore, increasing need for validating these emerging paradigms in multicentre trials. In this review, we focus on the tools commonly used to evaluate pulmonary arterial hyertension and also define some of the new approaches to pulmonary arterial hypertension.

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“…Synchronous right and left ventricular pressure measurements in patients with pulmonary arterial hypertension demonstrated a significant right-to-left transseptal pressure gradient at the time of maximal leftward septal displacement measured by magnetic resonance imaging (39). The mechanism behind this asynchrony is that right ventricular pressure overload leads to prolonged contraction of the right ventricular free wall (40). At the time that the left ventricle has entered its early diastolic phase, right ventricular pressure exceeds left ventricular pressure.…”

Section: Right Ventricular Failurementioning

confidence: 99%

Pulmonary Hypertension, Right Ventricular Failure, and Kidney

Schrier

Bansal

2008

Clinical Journal of the American Society of Nephrology

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In this article, the pathophysiology of left ventricular failure is reviewed. By contrast, the paucity of information about pulmonary arterial hypertension and right ventricular failure is acknowledged. The potential mechanisms whereby renal sodium and water retention in right ventricular failure secondary to pulmonary arterial hypertension can occur, despite normal left ventricular function, are discussed. With right ventricular failure as the primary cause of death in patients with pulmonary hypertension, more information about the mechanisms of renal sodium and water retention in these patients is direly needed. Specifically, studies to examine the activation of the neurohumoral axis at various stages of pulmonary arterial hypertension and right ventricular failure, including inhibition of mineralocorticoid and V2 vasopressin receptors, are indicated. Clin J Am Soc Nephrol 3: 1232-1237. doi: 10.2215 T he renal sodium and water retention that occurs with advanced left ventricular failure is associated with substantial morbidity and mortality. This sodium and water retention, which can lead to pulmonary edema, pleural effusion, and peripheral edema, occurs despite an increase in total blood volume. In normal individuals, a rise in total blood volume increases renal sodium and water excretion. The kidney is intrinsically intact with left ventricular failure, because the renal sodium and water retention does not persist after a successful heart transplant.This seeming paradox of increased blood volume yet renal sodium and water retention in cardiac failure has been explained by the body fluid volume regulation hypothesis (1-3). This hypothesis proposes that the kidney does not respond to changes in total blood volume but rather responds to what has been termed effective arterial blood volume. In general terms, approximately 85% of circulating blood volume is in the lowpressure venous side of the circulation, whereas only 15% is in the high-pressure arterial circulation. The integrity of the arterial circulation depends on cardiac output and systemic vascular resistance and is modulated by arterial stretch baroreceptors in the carotid sinus, aortic arch, and afferent arteriole of the glomerulus (4). Thus, despite an increase in total blood volume, arterial underfilling can occur secondary to a decrease in cardiac output in low-output heart failure or decreased systemic vascular resistance in high-output heart failure. With arterial underfilling secondary to either condition, arterial baroreceptor-mediated activation of the neurohumoral axis occurs. The resultant increase in renin-angiotensin-aldosterone system (RAAS) leads to sodium retention, and the increase in the nonosmotic release of arginine vasopressin (AVP) is associated with water retention and hyponatremia in advanced left ventricular failure, a known risk factor for increased mortality (5). This water retention is due to AVP activation of the V2 vasopressin receptors on the basolateral surface of the principal cells of the collecting duct, which increas...

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Interventricular Mechanical Asynchrony Due To Right Ventricular Pressure Overload in Pulmonary Hypertension Plays an Important Role in Impaired Left Ventricular Filling

Cited by 47 publications

References 5 publications

Right Versus Left Ventricular Failure

Right Versus Left Ventricular Failure

The value of tools to assess pulmonary arterial hypertension

Pulmonary Hypertension, Right Ventricular Failure, and Kidney

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