The Right Heart and Its Distinct Mechanisms of Development, Function, and Failure

Markel, Troy A.; Wairiuko, George M.; Lahm, Tim; Crisostomo, Paul R.; Wang, Meijing; Herring, Christine M.; Meldrum, Daniel R.

doi:10.1016/j.jss.2007.04.003

Cited by 27 publications

(35 citation statements)

References 114 publications

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“…Since ␣1-AR agonist catecholamines are elevated in heart failure, increased ␣1-AR inotropic responses in the RV myocardium may be adaptive in heart failure by helping the failing RV respond to increased pulmonary pressures. right ventricle; myosin light chain kinase; myofilament calcium sensitivy RIGHT VENTRICULAR (RV) failure is a prevalent cause of cardiovascular collapse and a major public health problem (14,20). RV failure frequently arises in patients with left ventricular (LV) failure and causes markedly worse symptoms and prognosis compared with patients with LV failure without RV dysfunction (9,11,13).…”

mentioning

confidence: 99%

Heart failure switches the RV α₁-adrenergic inotropic response from negative to positive

Wang

Yeh

Jensen

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Right ventricular (RV) failure is a serious common clinical problem that is poorly understood. Therefore, for failing and nonfailing hearts, we examined the distinctive inotropic responses induced in the RV myocardium after the stimulation of ␣ 1-adrenergic receptors (ARs). In RV trabeculae from nonfailing mouse hearts, ␣ 1-ARs induced a negative inotropic response, consistent with our previous study. In marked contrast, in RV trabeculae from failing hearts, 12 wk after coronary artery ligation, ␣1-ARs induced a positive inotropic response. Mechanistically, experiments with skinned trabeculae showed that ␣1-ARs decreased myofilament Ca 2ϩ sensitivity in the nonfailing RV myocardium, whereas ␣1-ARs increased Ca 2ϩ sensitivity in heart failure. This suggests that a switch in the Ca 2ϩ sensitivity response to ␣1-AR stimulation explained the switch in the RV ␣1-AR inotropic response in heart failure. Myosin light chain kinase (MLCK) can increase myofilament Ca 2ϩ sensitivity, and the smooth muscle isoform (smMLCK), which is also present in cardiomyocytes, was more abundant in the RV myocardium from failing versus nonfailing hearts. Moreover, the MLCK inhibitor ML-9 prevented the switch of the RV myocardium to a positive ␣1-AR inotropic response in heart failure. In the left ventricular myocardium, in contrast, ␣1-AR inotropic responses were not different in failing versus nonfailing hearts, and smMLCK abundance was not increased in heart failure. In relation to human disease, we found that smMLCK mRNA and protein levels were increased in RVs from failing human hearts. We conclude that the RV inotropic response to ␣1-ARs is switched from negative to positive in heart failure, through a pathway involving increased myofilament Ca 2ϩ sensitivity. Since ␣1-AR agonist catecholamines are elevated in heart failure, increased ␣1-AR inotropic responses in the RV myocardium may be adaptive in heart failure by helping the failing RV respond to increased pulmonary pressures. right ventricle; myosin light chain kinase; myofilament calcium sensitivy RIGHT VENTRICULAR (RV) failure is a prevalent cause of cardiovascular collapse and a major public health problem (14,20). RV failure frequently arises in patients with left ventricular (LV) failure and causes markedly worse symptoms and prognosis compared with patients with LV failure without RV dysfunction (9,11,13). Moreover, the prognosis of heart failure patients with pulmonary hypertension is strongly related to RV dysfunction (13).Despite its clinical significance, RV failure is relatively understudied and poorly understood (31). The RV has been viewed merely as a weak LV (14). Conversely, we (33) reported that the RV and LV have fundamentally different inotropic responses to stimulation of ␣ 1 -adrenergic receptors (ARs), which caused negative inotropic responses in the RV myocardium but positive inotropic responses in the LV myocardium. This and another study (31) have indicated that the RV and LV are categorically different and that RV failure cannot be understood by extrapola...

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mentioning

confidence: 99%

Heart failure switches the RV α₁-adrenergic inotropic response from negative to positive

Wang

Yeh

Jensen

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…In recent years, following the recommendations of the National Heart, Lung and Blood Institute (2006), various groups have focused on the study of the right ventricle [2,[6][7][8][9][10][11]. Along these lines, the present work shows a cross-sectional and global vision of right ventricular dysfunction at a specialized hospital center.…”

Section: Discussionmentioning

confidence: 96%

“…In recent years, the volume of scientific production focuses on the right ventricle has significantly increased [2,[6][7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 99%

Consecutive epidemiological study of right ventricular dysfunction at a reference hospital

Buendía-Fuentes¹,

Almenar‐Bonet²,

Vicente-Guillén³

et al. 2014

Cardio Vasc Syst

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Background and purpose: Right ventricular dysfunction (RVD) has been described as an independent factor for morbidity and/ or mortality in various nosological entities. However, there are no data on its true prevalence in hospital environments. The present study aims to discover the prevalence of this pathology at a specialized hospital center, as well as the characteristics of the patients affected. Methods and results: An observational and prospective study analyzing 7636 echocardiographs performed consecutively over a 20-month period. An etiological classification into four categories (cardiac cause, pulmonary thromboembolism, pneumopathy and idiopathic pulmonary hypertension) was proposed. 442 RVD cases were detected and classified, which is 5.78% of the examinations performed. Most of the cases (87.56%) presented prior cardiopathy as the origin of RVD. Only 12.44% presented a non-cardiac cause for RVD. Differences were detected in the demographic and echocardiographic characteristics of patients, depending on the etiology of the RVD. Conclusions: With a prevalence of 5.78% of all the echocardiographs performed in a specialized hospital, the significance of RVD is confirmed. The most frequent etiological factor for this disease is the existence of prior heart disease.

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“…The patho-physiology of RHF has been extensively studied and found to be most commonly caused by pulmonary embolism, acute cor-pulmonale, severe left ventricular failure, right ventricular infarction and in the setting sepsis [1][2][3][4][5][6]. One rarely encountered etiology of RHF is one-lung-ventilation (OLV) leading to insurmountable right heart strain.…”

Section: Introductionmentioning

confidence: 99%

One Lung Ventilation as a Cause of Obstructive Shock

Xu¹,

D’Souza²,

Kv³

et al. 2018

JCR

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Background: Right heart failure (RHF) in the intensive care setting is an underdiagnosed, yet serious condition that carries a significant morbidity and mortality. The patho-physiology of RHF has been extensively studied and found to be most commonly caused by pulmonary embolism, acute cor-pulmonale, severe left ventricular failure, right ventricular infarction and in the setting sepsis. One rarely encountered etiology of RHF is one-lung-ventilation (OLV) leading to insurmountable right heart strain. Case Report: A 62 year old presented with recurrent urinary retention secondary to prostatic hypertrophy. Computed Tomography of chest showed mass in left upper lobe. Endo-bronchial biopsy of mass in left lung resulted in pulmonary hemorrhage. OLV via selective ventilation of only the right lung was employed which resulted in pulmonary hypertension and shock. Conclusion: We believe that in a hypotensive patient undergoing OLV, the practitioner must consider the possibility of obstructive shock secondary to the right heart strain generated by this technique. If RHF is suspected, we recommend obtaining an echocardiogram to detect signs of right heart strain. If strain in present, OLV must be stopped while the patient returns to hemodynamic stability. Further studies regarding the role of one lung ventilation as a cause of obstructive shock will be helpful.

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The Right Heart and Its Distinct Mechanisms of Development, Function, and Failure

Cited by 27 publications

References 114 publications

Heart failure switches the RV α₁-adrenergic inotropic response from negative to positive

Heart failure switches the RV α₁-adrenergic inotropic response from negative to positive

Consecutive epidemiological study of right ventricular dysfunction at a reference hospital

One Lung Ventilation as a Cause of Obstructive Shock

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The Right Heart and Its Distinct Mechanisms of Development, Function, and Failure

Cited by 27 publications

References 114 publications

Heart failure switches the RV α1-adrenergic inotropic response from negative to positive

Heart failure switches the RV α1-adrenergic inotropic response from negative to positive

Consecutive epidemiological study of right ventricular dysfunction at a reference hospital

One Lung Ventilation as a Cause of Obstructive Shock

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Heart failure switches the RV α₁-adrenergic inotropic response from negative to positive

Heart failure switches the RV α₁-adrenergic inotropic response from negative to positive