Pulmonary Hypertension in Candidates for Bariatric Surgery: A Cause for Concern

by Peter N. Benotti, MD

Dr. Benotti is from The Obesity Institute, Geisinger Medical Center, Danville, Pennsylvania.

Bariatric Times. 2013;10(8):14–17.

FUNDING: No funding was provided.
DISCLOSURES: The author reports no conflicts of interest to the content of this article.

ABSTRACT
Pulmonary hypertension has recently been indentified as a risk factor for adverse events and mortality after gastric bypass surgery. This condition can be present in association with obstructive sleep apnea, obesity hypoventilation, obese cardiomyopathy, and chronic thromboembolism. Since this is a modifiable risk factor and may be overlooked in the evaluation of bariatric candidates, bariatric surgeons and team members should become more familiar with guidelines for current diagnosis, prognosis assessment, and treatment. Improved diagnosis and severity assessment will enhance the patient selection and optimization process in bariatric surgery.

Introduction
Extreme obesity is often accompanied by varying degrees of pulmonary hypertension (PH). Often when this diagnosis is made or is suspected in bariatric surgery candidates, consultants are engaged to provide guidance regarding clinical significance, additional workup, and management. These consultants frequently indicate that the best treatment for PH with extreme obesity is weight loss, and that additional study is unnecessary because it will not change management. Several recent studies utilizing a large clinical bariatric surgery registry have identified PH as a risk factor for both composite adverse outcomes1 and 30-day mortality[2] following bariatric surgery. This observation justifies a closer look at this condition and how it might influence the evaluation and selection of candidates for bariatric surgery. A recent advisory from the American Heart Association, which addresses the evaluation and management of patients with severe obesity undergoing surgery, calls attention to a number of clinical findings that are likely to influence cardiac assessment and management (Table 1).[3]

Discussion: Diagnosis and Management of PH
Pulmonary hypertension is defined as a mean pulmonary artery pressure that exceeds 25mmHg on right heart catheterization. This condition can occur as a primary disease or as a physiologic consequence of another condition or conditions. The current classification scheme for PH is summarized in Table 2.[4-7]

Obesity and its comorbid conditions are significant contributors to secondary pulmonary hypertension (Groups 2–4). There is limited information regarding the prevalence of PH in extreme obesity. The reported incidence in the Bariatric Outcomes Longitudinal Database (BOLD), which is the largest clinical registry in bariatric surgery, is 0.4 percent.[1,2] However, this may be an underestimate since a single institution cohort study found that 28 percent of otherwise healthy individuals with a body mass index (BMI) more than 30kg/m2 had a pulmonary artery systolic pressure (PAS) > 30mmHg by echocardiography.[8] Among a cohort of 220 consecutive patients with obstructive sleep apnea (OSA), the prevalence of PH confirmed by invasive direct measurement was 17 percent.[9] Within these small studies, BMI was found to correlate with the prevalence of PH. Although the data from BOLD suggest that the prevalence of PH is low, it is likely that the actual prevalence of significant PH is higher among candidates for bariatric surgery because the diagnosis is often overlooked or missed.

The clinical symptoms of PH are non-specific. They include dyspnea and syncope with exertion, palpitations, and leg edema. Clinical signs are unreliable in extreme obesity because of the huge subcutaneous fat thickness. They include loud second heart sound (P2), murmur of tricuspid regurgitation, giant v waves, and a pulsatile liver. More advanced cases are accompanied by signs of right ventricular failure. In extreme obesity the pathogenesis of PH depends on the contributing comorbid conditions. OSA (Group 3) is accompanied by repetitive nocturnal hypoxia and increased sympathetic activity, which induces pulmonary artery vasoconstriction. Repeated pulmonary vasoconstriction leads to pulmonary arteriolar remodeling, including intimal proliferation, medial hypertrophy, and other changes that increase pulmonary vascular resistance.[4] In obesity hypoventilation syndrome (OHS), pulmonary artery vasoconstriction is stimulated by hypoxia, hypercarbia, and acidosis with subsequent arteriolar remodeling. In OHS, pulmonary hypertension tends to be more common and more severe than in OSA.[10]

PH related to left heart disease (Group 2) is the most common etiology when PH is diagnosed by echocardiography.[4] In extreme obesity, especially of longer duration, alterations in cardiac structure and function are common. The increase in body mass and oxygen consumption in extreme obesity result in increased circulatory demands, which include an increase in cardiac output, stroke volume, and stroke work. The increased cardiac demand gradually results in cardiac chamber dilatation and increased ventricular wall stress. In order to maintain cardiac performance in the presence of increased wall stress, eccentric cardiac hypertrophy develops. This gradually results in increased ventricular wall thickness and diminished ventricular compliance. The “stiff” left ventricle causes abnormalities in ventricular diastolic filling. The progressive diastolic dysfunction causes increases in left ventricular filling pressures, which contributes to increased pulmonary artery pressures. This often progresses to diastolic heart failure with preservation of left ventricular systolic function, which is common in longstanding extreme obesity.[11]

Systolic function will eventually deteriorate when the hypertrophied left ventricle can no longer compensate for the chamber dilation and increased wall stress. Systolic dysfunction worsens the elevation in left ventricular filling and pulmonary artery pressures. These structural and functional changes in the heart, which occur in extreme obesity, are termed the obese cardiomypoathy, a condition that is present in 31 percent of individuals with extreme obesity, especially those with longstanding obesity.12 One of the exciting observations for bariatric surgeons is that these cardiac alterations are largely reversible with surgical weight loss.[13,14]

Another obesity-related etiology of secondary PH is chronic thromboembolic disease (Group 4). This condition is present in four percent of patients from the general population followed for two years after surviving a pulmonary embolus.[15]   It is probably more common in extreme obesity, a proven risk factor for thromboembolism, where other comorbid conditions like OSA and diastolic dysfunction are likely to contribute to PH. Incomplete clot resolution or recurrent thromboembolism causes an increase in pulmonary artery pressure, pulmonary vascular resistance, and right ventricular strain. The links between extreme obesity and venous thrombosis are numerous and include increased levels of plasminogen activator Inhibitor-1 ((PAI-1), increases in circulating procoagulant micro-particles, endothelial dysfunction, increased production of inflammatory cytokines, and increased levels of clotting factors.[16]

Transthoracic echocardiography is currently used as a screening tool for PH. This modality provides a calculated estimate of pulmonary artery systolic pressure. However, this noninvasive test has significant limitations, which relate to technical issues and interobserver variability.[4,5,17]  In the clinical setting, significant differences occur between noninvasive estimates and invasive measurements of pulmonary artery systolic pressure. Echocardiography can provide important information about systolic and diastolic function of the left and right ventricles.[18] In PH, the level of right ventricular function is a major determinant of prognosis and risk.[4,5,17] Because of the limitations of echocardiography, established guidelines for diagnosis and management of PH require confirmatory invasive diagnostic testing for both the diagnosis of PH and for information regarding the classification and prognosis, which facilitates treatment and risk assessment.[10,17] Right heart catheterization provides direct measurement of PA pressures, calculation of vascular resistance, measurement of pulmonary capillary wedge pressure (PCWP), and cardiac index. A PCWP more than 15 identifies PH related to left heart disease (Group 2), and a PCWP of 15 or less will identify patients with hypoxia (Group 3) or chronic thromboembolism
(Group 4).[4-6,10,17]

Additional testing necessary for the diagnosis and evaluation of PH are listed in Table 3.[4-6,10,19[
If the diagnosis of PH is confirmed and the evaluation complete, the prognosis and possible treatment options should be determined. The prognosis in PH is determined by the information from right heart catheterization (CVP, PA pressures, and cardiac index), and a functional assessment, most commonly, the six-minute walk test.20,21 A low cardiac index, evidence of right ventricular failure, and poor functional state are ominous prognostic signs for patients with PH.[5,10,18,19]

Conclusion
The above summary of the evaluation and management of PH is taken from review of the current medical literature for the benefit of bariatric surgery teams because of the recent findings that PH is a risk factor for adverse events and 30-day mortality after bariatric surgery. There are currently no guidelines for the evaluation and management of PH in bariatric surgery candidates. Bariatric surgeons should be familiar with current management of PH and other serious comorbid conditions in order to communicate and collaborate with medical specialist consultants in the work-up, evaluation, and management of high-risk conditions like PH. Improved collaboration should generate recommendations for the extent of work-up and treatment required. Since this potentially modifiable condition is associated with risk in bariatric surgery, cardiologists skilled in echocardiography should carefully evaluate bariatric surgery candidates at risk for PH, such as those with severe OSA, obesity hypoventilation, thromboembolism, and obese cardiomyopathy.

If the diagnosis of PH is suspected, its severity and prognosis should be assessed with right heart catheterization, measurement of cardiac output, and functional assessment. The hemodynamic data from right heart catheterization under basal conditions and good oxygenation may also help direct perioperative fluid and/or diuretic management using right atrial pressure monitoring during the perioperative period. Hopefully, this comorbid condition will be the subject of clinical investigation in bariatric surgery programs, which should provide improved diagnosis and management guidelines for this condition.

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