The Transition From Hypertension to Heart Failure : Contemporary Update
Temple Health's Heart And Vascular Institute Reaches Specialty Milestone
Philadelphia-based Temple University Hospital has achieved twin milestones in the treatment of chronic thromboembolic pulmonary hypertension. Care teams from the Advanced Pulmonary Hypertension, Right Heart Failure and CTEPH program at Temple's Heart and Vascular Institute have completed their 500th pulmonary thromboendarterectomy and 500th balloon pulmonary angioplasty.
Temple University Hospital is home to the largest CTEPH center in the eastern U.S., with pulmonary thromboendarterectomies only performed at a handful of hospitals across the nation, according to an Aug. 21 news release from the health system.
CTEPH is a potentially fatal form of high blood pressure "in the circulation of the lungs resulting from a blood vessel that has been blocked by a prior pulmonary embolism," the release said.
Pulmonary thromboendarterectomy involves placing the patient on a heart-lung machine and cooling their body to 65 degrees to periodically pause circulation. Pulmonary angioplasty remains an option for patients who are not eligible for a pulmonary thromboendarterectomy.
Temple University Hospital's pulmonary thromboendarterectomy survival rate is 95%, according to the release.
Anjali Vaidya, MD, director of the Advanced Pulmonary Hypertension, Right Heart Failure and CTEPH program at Temple University Hospital shared more about the dual achievement with Becker's.
Editor's note: Responses have been lightly edited for clarity and length.
Question: What do these twin milestones reveal about Temple's efforts to build a nationally recognized center of excellence?
Dr. Anjali Vaidya: Temple Heart and Vascular has been committed to our goal of providing exceptional care to each individual patient. Our nationally recognized pulmonary hypertension center of excellence is a testament to years of specialized pulmonary hypertension careers with emphasis on advanced clinical care, scholarly innovation and vast educational outreach.
Q: What were the most critical decisions or investments that enabled Temple to become the largest CTEPH center in the Eastern U.S.?
AV: Our team's commitment to meticulous clinical care with exceptional outcomes, with interdisciplinary collaborations between cardiology and Dr. Yoshiya Toyoda's [MD, PhD] cardiovascular surgery team.
Q: What has been most important to sustaining the interdisciplinary model at Temple's pulmonary hypertension program?
AV: Our team works extremely well together across departments, all with a patient-centered approach. We learn from each other and grow our experiences in partnership across cardiology, cardiac surgery, interventional cardiology, anesthesiology, radiology and more. The collaborative model at Temple allows for the best patient experiences and outcomes.
Q: Looking ahead, what innovations or research directions will shape the next phase of the program?
AV: Our team is continuously innovating on the scholarly front, inspired by and building on our clinical experiences and incorporating novel therapeutic techniques. The integration of multimodality treatments for an individual patient's CTEPH management continues to evolve, and being at the forefront of this with colleagues around the world has been exceptionally rewarding and beneficial for our patients.
Moves In Medicine: Diagnosing CTEPH Before It's Too Late
A groundbreaking program boasts the most expertise on the East Coast for a condition that's often misdiagnosed. And that condition could be life threatening.
Tara Cottee's doctor said her heart function looks perfect now. That's her story today, but six years ago she was tethered to an oxygen tank at just 34-years-old.
"Even with the oxygen I still couldn't breathe good," she said.
Misdiagnosed with a sinus infection, she said she became alarmed when she started coughing up blood. That's when she sought help from Dr. Paul Forfia, co-director of Temple Health's CTEPH Program.
CTEPH stands for Chronic Thromboembolism Pulmonary Hypertension. "This is a condition where there's elevated blood pressure in the lungs related to residual blood clot in the lung leftover from a pulmonary embolism," said Dr. Forfia.
A pulmonary embolism is when a blood clot that developed in the legs or pelvis, breaks off, travels through the body and gets lodged in the lungs.
"On blood thinners about 95 percent of people will have their clots clear from their lungs over time, usually by about three months," said Dr. Forfia.
It's that last five percent who Dr. Forfia said will develop CTEPH.
Cottee had had a previous pulmonary embolism. She said following surgery with Forfia's team, she's a new person.
"I mean little things, you know, little just walking across the room just being able to breathe in general without oxygen," she said. "In Tara's case she had total reversal of pulmonary hypertension, total reversal of her right sided heart failure and restoration of a normal quality of life within a matter of days to weeks," explained Dr. Forfia.
Temple said CTEPH isn't rare, it's just tough to diagnose.
"CTEPH more than any other form of heart failure that I care for is the most complex in terms of diagnosis and evaluation," said Dr. Anjali Vaidya, who is also a co-director of the CTEPH program.
That mean's going to the experts. Temple Health is the second largest CTEPH program in the country and the only one on the East Coast.
"The delay in diagnosis is really a problem that so many of our patients suffer from and often its years before the accurate diagnosis is made," said Dr. Vaidya.
Coming up in the next healtcheck, Temple's CTEPH program recently saved the life of a man who collapsed on the job in Washington D.C. It was all thanks to a phone call that doctor knew to make.
Clinical Impact Of Mean Pulmonary Arterial Pressure After Balloon Pulmonary Angioplasty For Inoperable Chronic Thromboembolic Pulmonary Hypertension
This study investigated the effects of mPAP after BPA on clinical outcomes and long-term prognosis. We compared clinical parameters, withdrawal from pulmonary vasodilators or oxygen therapy and prognosis across three groups: mPAP≤20, >20–<30 and ≥30 mm Hg. Key findings were: (1) patients with mPAP ≤20 mm Hg showed greater improvements in symptoms, exercise tolerance, plasma BNP levels and RVEF. (2) Fewer patients in this group continued treatment with pulmonary vasodilators and oxygen therapy. (3) Although patients with mPAP <30 mm Hg had a favourable long-term prognosis, outcomes were similar between the mPAP ≤20 mm Hg and >20–<30 mm Hg groups.
In this study, the overall prognosis after BPA was favourable, although a small number of patients did not achieve the general treatment goal of an mPAP of <30 mm Hg. The group with an mPAP of ≥30 mm Hg had a significantly poorer prognosis than the other groups, which is similar to the findings of previous reports describing the natural history of CTEPH.22 Patients who achieved an mPAP of <25 mm Hg after BPA were reportedly less likely to experience recurrent pulmonary hypertension and had a better prognosis.21 In the current study, prognosis was similar between groups with an mPAP of ≤20 mm Hg and >20–<30 mm Hg. This suggests that mild pulmonary hypertension after BPA is acceptable for selected patients—such as older individuals with reduced activity and those unable to undergo frequent treatment due to psychiatric or other disorders—when the primary goal is to improve prognosis rather than to relieve symptoms or improve exercise tolerance. However, since the results may not have been fully adjusted for patient background, the findings should be interpreted cautiously. Although the median observation period was 44 months, it might still be insufficient for assessing the long-term prognosis of patients with mild pulmonary hypertension.
The group with normalised haemodynamics after BPA (a group with an mPAP of ≤20 mm Hg) had milder symptoms, better exercise tolerance, lower plasma BNP levels and a higher RVEF. This suggests that BPA aimed at lowering mPAP leads to improved clinical parameters, including symptoms, exercise tolerance and right ventricular function. The decrease in mPAP after BPA may have reduced afterload in the right heart system and contributed to the improvements in symptoms and exercise tolerance. Although no trend in the CI, considered a factor contributing to exercise tolerance, was found across the three groups, the heart rate was lower in the group with a lower mPAP than in the other groups. On CMR images, no trends in right ventricular end-diastolic volume index or right ventricular stroke volume index were found across the three groups; however, RVEF was better in the lower mPAP group than in the other groups, reflecting a decrease in afterload. However, further research is required to determine whether this favourable RVEF and low resting heart rate are beneficial during exercise. Some reports indicate that improvement in resting mPAP alone is insufficient to improve symptoms and exercise tolerance.23 A previous report suggested that although resting mPAP did not correlate with 6MWD, peak oxygen consumption in exercise testing correlated with 6MWD.24 However, the present study did not evaluate exercise-induced pulmonary hypertension, and it may be insufficient to evaluate symptoms and exercise tolerance based on resting haemodynamic assessment alone.
Fewer patients with lower mPAP required oxygen therapy or pulmonary vasodilators. We speculate that improved oxygenation and haemodynamics in this group prompted treatment withdrawal. Given that oxygen therapy restricts daily life, achieving an mPAP of ≤20 mm Hg—and thus reducing treatment reliance—may enhance the quality of life. However, as treatment withdrawal was at each physician's discretion, the findings may not be generalisable. In Japan, pulmonary vasodilators, including riociguat25 and selexipag,26 are used to treat microvasculopathy in patients with CTEPH. A recent report suggests that pulmonary vasodilators after BPA are effective, particularly in older patients,27 and further studies are warranted to determine the criteria for the continuation or discontinuation of pulmonary vasodilators after BPA.
This study explored the clinical impact of mPAP after BPA and suggested goals for mPAP after BPA. Normalisation of mPAP after BPA is required to improve clinical parameters, such as symptoms and exercise tolerance. A previous report has shown that additional BPA after BPA treatment can be safely performed and can improve symptoms and 6MWD.28 In cases of mild pulmonary hypertension—defined as an mPAP >20–<30 mm Hg with lesions suitable for additional BPA—further BPA may be considered to improve symptoms and exercise tolerance. Further studies are needed to assess the haemodynamic benefits of adding pulmonary vasodilators in patients without BPA-treatable lesions. Moreover, depending on the patient's daily activities and treatment tolerability, mild pulmonary hypertension with an mPAP >20–<30 mm Hg after BPA may be acceptable solely to improve prognosis. Consequently, BPA treatment should be tailored to the individual patient's condition.
Study limitationsThis study has some limitations. First, this was a single-centre retrospective study with few cases, limiting the generalisability of its findings; thus, prospective multicentre studies are needed. Second, although the findings suggest an association between mPAP after BPA and clinical parameters as well as long-term prognosis, establishing a causal relationship between BPA-induced mPAP reduction and these outcomes was hindered by inadequate adjustment for patient background and other factors. Moreover, as an exploratory study, robust causal inferences were inherently challenging. Third, this study included only patients who underwent follow-up RHC, and 53 patients were excluded for this reason. Among these excluded patients, 11 died during the follow-up period, raising the possibility that selection bias cannot be completely ruled out. In the analytic cohort (n=304), pneumonia and unknown cause were frequent among the 13 deaths; by contrast, in the excluded group (n=53), of the 11 deaths only one was due to pneumonia and two were of unknown cause. The remaining causes included malignancy (n=4), ischaemic heart disease (n=1), senility (n=1), cellulitis (n=1) and intestinal obstruction (n=1). This distribution suggests that deaths in the excluded cohort were not predominantly attributable to CTEPH, and comorbidities may have limited the feasibility of follow-up RHC. Fourth, CMR images were performed as close as possible to the first follow-up RHC, with a median interval of 0 months (IQR 0–2). However, the variability in timing between CMR and RHC may have led to inconsistencies in the assessment of right ventricular function relative to haemodynamic status, potentially introducing measurement bias. Finally, the criteria for withdrawing oxygen therapy and pulmonary vasodilators were unclear and based on each physician's discretion.
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