49.11 Cardiac conditions in peripheral arterial diseases

This section was reviewed and edited by The Task Force for the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) Authors/Task Force Members: Helmut Baumgartner (ESC Chairperson) (Germany), Volkmar Falk (EACTS Chairperson) (Germany), Jeroen J. Bax (The Netherlands), Michele De Bonis (Italy), Christian Hamm (Germany), Per Johan Holm (Sweden), Bernard Iung (France), Patrizio Lancellotti (Belgium), Emmanuel Lansac (France), Daniel Rodriguez Muñoz (Spain), Raphael Rosenhek (Austria), Johan Sjögren (Sweden), Pilar Tornos Mas (Spain), Alec Vahanian (France), Thomas Walther (Germany), Olaf Wendler (UK), Stephan Windecker (Switzerland), Jose Luis Zamorano (Spain)

Cardiac conditions other than CAD are frequent in patients with PADs. This is especially the case for heart failure and atrial fibrillation in patients with LEAD. In patients with symptomatic PADs, screening for heart failure should be considered. In patients with heart failure, screening for LEAD may be considered. Full vascular assessment is indicated in patients planned for heart transplantation or cardiac assist device. In patients with stable PADs who have AF, anticoagulation is the priority and suffices in most cases. In the case of recent endovascular revascularization, a period of combination therapy (anticoagulant + antiplatelet therapies) should be considered according to the bleeding and thrombotic risks. The period of combination therapy should be as brief as possible. In patients undergoing transcatheter aortic valve implantation or other structural interventions, screening for LEAD and UEAD is indicated.

Cardiac diseases are frequent in patients with PADs. The simultaneous presence of PADs and CAD is addressed in Chapter 49.10. Here, we address the most important issues related to PADs patients with coexisting heart failure, AF, and valvular heart disease. Such coexistence may carry important prognostic and therapeutic implications and often needs a multidisciplinary approach.

There are multiple pathways linking LEAD and heart failure (Figure 49.11.1). Together with diabetes, smoking, and other risk factors, inflammation may be one of the common factors leading to the development of heart failure in PADs patients.¹ Data on the coexistence of the two conditions are generally limited to subjects with heart failure and LEAD.

LEAD is associated with increased risk for incident heart failure. It is often associated with overt atherosclerosis involving CAD, which may cause subsequent heart failure.² In addition, elevated aortic stiffness increases left ventricular (LV) afterload and high pulse pressure impairs coronary blood flow, resulting in hypertension, LV hypertrophy and diastolic dysfunction, and ultimately heart failure.^3,4 Importantly, skeletal muscle involvement and deconditioning in LEAD may affect heart failure severity.^5,6 On the other hand, functional limitation due to heart failure is likely to mask symptoms of LEAD, causing underestimation of the number of patients with both conditions.

Overall, LV dysfunction and heart failure are more frequent in patients with PADs. The evidence is mostly presented in patients with LEAD (see Chapter 37.1).

One-third of patients with symptomatic PADs have reduced LV ejection fraction.^7,8 LV dysfunction is at least twice as prevalent in patients with LEAD as in the general population, matched for age and sex.^8,9,10 This association with LV dysfunction may be even stronger for carotid artery disease than for LEAD.⁹ In a community-based study with participants over 65 years of age, an ankle–brachial index (ABI) less than 0.90, as compared to 0.90 or greater, increased the relative risk for incident heart failure by 1.61 (95% confidence interval (CI) 1.14–2.29) over a 6-year follow-up period. However, this increase was not observed among patients with prevalent CAD.¹¹ In a population of older adults followed for a median of 7.5 years, the multivariable-adjusted hazard ratio (HR) for heart failure with symptomatic LEAD was 3.92 (95% CI 2.13–7.21).¹² Also in a younger population with cardiovascular (CV) disease or high CV risk, the incidence of heart failure was higher in patients with an ABI less than 0.90, as compared to 0.90 or greater (4.6% vs 2.6%).² In a large, middle-aged population with an 18-year follow up, incident cases of heart failure occurred in 23% of patients with an ABI less than or equal to 0.90, compared to 18%, 13%, and 14% of patients with an ABI of 0.91–1.00, 1.01–1.40, and greater than 1.40, respectively.¹³ These associations persisted after adjustment for carotid plaques, CAD, and other risk factors for heart failure. The multivariable-adjusted population attributable risk for incident heart failure by an ABI of 1.00 or less was 6%, compared to 8% for CAD, 15% for hypertension, and 14% for diabetes.¹³

Despite the high prevalence and incidence of heart failure in patients with PADs, outcome data for this group are very limited. It is most likely, however, that this combination is associated with increased CV morbidity and mortality. Evaluation of LV function in PADs may be of value for a better risk stratification for future CV events and a comprehensive management of patients’ CV diseases.⁹ This is particularly important when an intermediate- or high-risk vascular intervention is planned.¹⁴ The primary assessment should include medical history, physical examination, and resting electrocardiogram. In case of any abnormalities suggestive of heart failure, transthoracic echocardiography (TTE) or measurement of natriuretic peptides should be undertaken.¹⁵ Natriuretic peptides are particularly useful in patients with a poor echocardiographic window and in those with diastolic dysfunction.¹⁶ In patients with LEAD, heart failure may be associated with reduced patency after endovascular therapy.¹⁷ TTE and natriuretic peptides can also be proposed in patients with claudication, even if no revascularization is planned.

Observational studies and meta-analyses consistently show that the presence of LEAD in heart failure patients is an independent predictor of hospitalizations and mortality.^18,19,20,21 In the Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training (HF-ACTION) study, LEAD was reported in around 7% of patients with heart failure and LV ejection fraction less than 35%, and was associated with an increased risk of all-cause hospitalization and mortality (HR 1.31; p = 0.011).²⁰ Other studies reported an increased risk for progressive heart failure (HR 1.35; p = 0.03), all-cause mortality (HR 1.36; p <0.001),²² and CV mortality (HR 1.31; p = 0.02).²³ Among hospitalized patients with heart failure, the prevalence of subclinical (ABI ≤0.90) and symptomatic LEAD was 19% and 7%, respectively, and was associated with increased cardiac and all-cause mortality.²¹ Therefore, in heart failure patients, screening for PADs may be considered.

Finally, flash pulmonary oedema may be due to severe renal artery stenosis (see ‘Clinical presentation’ in Chapter 49.8). Therefore, in patients with this condition, testing for renal artery stenosis may be considered.

Ageing is a strong risk factor for AF²⁴ and PADs. Thus, a frequent coexistence of the two conditions is expected. In an analysis from the Cardiovascular Health Study, LEAD was associated with a higher risk of AF (HR 1.52; p <0.01).²⁵

Despite a considerable variability in blood pressure due to the beat-to-beat variability in stroke volume, ABI appears to be a reliable method to detect unknown LEAD in patients with AF.²⁶ In patients with AF receiving anticoagulant treatment, abnormal ABI was an independent predictor of all-cause death and major bleeding complications.²⁷

Among 41,882 patients hospitalized for LEAD, the prevalence of AF was 13%.²⁴ Those with AF tend to be older, more often hypertensive, female, with diabetes, chronic kidney disease, CAD, and/or heart failure, than patients in sinus rhythm. LEAD was overall more severe in patients with AF, as assessed by the Rutherford classification. In-hospital complications, including renal failure, myocardial infarction, stroke, infections, and death, occurred more frequently in the presence of AF. In other studies, AF associated with LEAD was an independent predictor of stroke, amputation, and death.^28,29 In the REACH registry, AF was present in 10% of patients with LEAD.³⁰ Compared with patients without AF, the 2-year CV and all-cause mortality was higher, 7.7% and 5.6% versus 2.5% and 1.6%, respectively (p < 0.001 for both). Those with AF also had higher incidences of heart failure, unstable angina, and severe bleeding.

Except for recent stenting, patients with PADs and AF should mostly be under oral anticoagulants alone (see Chapter 6.9–6.12). See ‘Antithrombotic therapy in lower extremity artery disease patients requiring long-term oral anticoagulant’ in Chapter 49.4.

PADs are common among patients with valvular heart disease, especially among the elderly with symptomatic aortic stenosis (see Chapter 35.3). The presence of LEAD is captured within the scores used to predict outcome after cardiac surgery.³¹ Among patients with symptomatic aortic stenosis not eligible for surgical aortic valve replacement, the prevalence of LEAD is as high as 40%.^32,33,34 It often coexists with other manifestations of systemic atherosclerosis, including CAD and cerebrovascular disease. This has an impact on patient care with respect to the timing of coronary revascularization if needed,³⁵ and the vascular access site for TAVI.³⁶ Systematic computed tomography scan imaging of the aorta, including all major peripheral arteries, has become the standard of care in patients eligible for TAVI.

Patient evaluation for the presence of LEAD and UEAD is pivotal for access site choice in patients eligible for TAVI, and their diagnosis has a great impact on clinical outcome after TAVI because of the increased rate of peri- and post-procedural complications.^34,38 The presence of LEAD or UEAD is an independent predictor of mortality following TAVI with both percutaneous and surgical access, independent of the occurrence of vascular complications.^37,38,39 The use of low-profile devices for TAVI and alternative access sites, such as direct aortic, carotid, or subclavian, may also reduce vascular complications.

Acute limb ischaemia is a complication of intra-aortic balloon pump insertion in the setting of cardiogenic shock or in the prophylaxis of the low-output syndrome. LEAD is a major risk factor for this complication, and preliminary iliac artery stenting with the use of an unsheathed device may avoid such complications.⁴⁰ These complications are also common in LV assist device recipients, where sheaths are usually larger, resulting in higher 30-day mortality in patients with LEAD.⁴¹ The added risk of underlying LEAD is not clearly established in that particular setting and deserves additional investigations. These patients often need lower limb revascularization and surgical vascular closure when weaned off LV assist devices.

See Table 49.11.1 for recommendations on the management of cardiac conditions associated with peripheral arterial diseases.