Overview of Vascular Disease

Background

Vascular diseases are a heterogeneous group of conditions involving arteries, veins, and lymphatic vessels. Collectively, they represent one of the leading causes of death and disability worldwide. According to the Global Burden of Disease (GBD) study, ischemic heart disease and stroke remain the top two causes of mortality, while peripheral artery disease (PAD), aneurysmal disease, and venous thromboembolism (VTE) contribute to major morbidity (GBD 2019)📄^,(Benjamin 2019)📄^,(Gornik 2024).

The prevalence of vascular diseases is rising with population aging, increased prevalence of diabetes mellitus, hypertension, obesity, and smoking (Criqui 2015)📄^,(Fowkes 2013). In high-income countries, improved survival after myocardial infarction and stroke has also resulted in more patients living with chronic vascular conditions. In low- and middle-income countries, the burden is shifting rapidly, often without adequate access to specialized care, necessitating robust regional cardiovascular disease (CVD) prevention and risk assessment strategies (Al 2025).

Epidemiological studies, such as those from Fowkes et al. on PAD (Fowkes 2013), and registries like Swedvasc and Vascunet, demonstrate that vascular disease is not only common but also associated with high long-term mortality and limb loss. Contemporary guidelines from the European Society for Vascular Surgery (ESVS) and Society for Vascular Surgery (SVS), as well as joint statements from the American College of Cardiology (ACC) and American Heart Association (AHA), emphasize integrated management — prevention, early diagnosis, and individualized treatment plans (ESVS 2024)^,(Chaikof 2018)📄^,(Gornik 2024).

Arterial Disease

Atherosclerosis is the predominant etiology of arterial disease. It results from a complex interplay between endothelial dysfunction, lipid deposition, chronic inflammation, and thrombosis. Established risk factors include:

• Modifiable: smoking, hypertension, diabetes, dyslipidemia, obesity, and a sedentary lifestyle.
• Non-modifiable: age, sex, family history, genetic disorders.

Inflammatory mediators (interleukin-6, C-reactive protein) and lipid abnormalities (high low-density lipoprotein [LDL], low high-density lipoprotein [HDL]) play central roles (Libby 2021). Management of modifiable risk factors is paramount; for instance, structured exercise programs and the integration of patients with peripheral artery disease (PAD) into cardiac rehabilitation are recommended to address physical inactivity (Feka 2026).

Aneurysmal Disease

Abdominal aortic aneurysm (AAA), thoracic aortic aneurysm (TAA), and peripheral aneurysms (popliteal, visceral) develop due to degeneration of vascular wall connective tissue. Smoking is the most consistent modifiable risk factor for AAA, conferring a 5-fold increased risk (Sakalihasan 2018). Recent epidemiological data highlight the continued global burden of aortic disease, with significant variations in prevalence based on age and sex (Martin 2025), (Tessarek 2023). Beyond clinical outcomes, there is an increasing recognition of the impact of AAA on patient quality of life, necessitating the integration of patient-reported outcomes (PROs) into clinical assessment to address evolving dynamic patient needs (Smolderen 2026), (Smolderen 2026), (Smolderen 2026). Familial clustering suggests genetic predisposition, and current guidelines emphasize the importance of genetic screening in patients with thoracic aortic disease (Isselbacher 2022)📄, (Isselbacher 2022), (Isselbacher 2022). Systematic reviews supporting society guidelines, including those from the Society for Vascular Surgery (SVS), reinforce the need for specialized management and surveillance in heritable thoracic aortic disease (HTAD) to prevent catastrophic events (Firwana 2023), (Firwana 2023), (Firwana 2023). Connective tissue disorders such as Marfan, Loeys-Dietz, and Ehlers-Danlos syndromes are strongly associated with TAA and dissection (Rutherford 2018), (Isselbacher 2022)📄.

> See Also: 4Ch. 4: Aneurysmal Diseases for detailed management of AAA, TAA, and peripheral aneurysms.

Thromboembolic Disease

Virchow's triad — endothelial injury, venous stasis, and hypercoagulability — remains the conceptual framework (Rutherford 2018). Recent evidence suggests that venous stasis may lead to DVT through venous valve hypoxia, which triggers a pro-thrombotic microenvironment even in the absence of overt endothelial denudation (Shaydakov 2024).

• Acquired risks: trauma, surgery, malignancy, immobility, oral contraceptives, pregnancy.
• Inherited thrombophilia: Factor V Leiden, prothrombin gene mutation, protein C/S deficiency.

While traditionally viewed as embolic, emerging data in trauma patients suggest that some pulmonary thromboemboli may develop de novo within the pulmonary vasculature, challenging the paradigm that all PE originates from lower extremity DVT (Knudson 2022).

> See Also: 12Ch. 12: Venous Thromboembolism for comprehensive VTE prevention, diagnosis, and treatment.

Venous Disease

Chronic venous disease (CVD) often follows prior deep vein thrombosis (DVT) with valvular destruction and reflux. Congenital venous malformations and primary valvular incompetence also contribute. Venous hypertension leads to edema, pigmentation, lipodermatosclerosis, and ulceration (Greenhalgh 2010)📄.

Table 1.1. Major Risk Factors for Vascular Disease

Use CEAP for standardized reporting (C1–C6 with etiologic, anatomic, pathophysiologic domains) and VCSS for severity. Post-thrombotic syndrome and primary valvular reflux share a final common pathway of venous hypertension leading to skin changes and ulceration (Ekl 2004)📄^,(Kahn 2014)📄.

> See Also: 13Ch. 13: Chronic Venous Insufficiency for detailed venous disease management including CEAP classification applications.

Atherosclerosis

Endothelial dysfunction allows low-density lipoprotein (LDL) to penetrate the intima, where it undergoes oxidation. Monocytes adhere, migrate, and differentiate into macrophages, forming foam cells. Smooth muscle proliferation and extracellular matrix deposition lead to fibrous cap formation. Plaque rupture triggers platelet activation and thrombus formation, which can result in acute ischemic events (Libby 2021). Given the central role of LDL in this process, lipid-lowering therapy is foundational to management, although real-world adherence to statin therapy remains a significant clinical challenge influenced by various patient and provider determinants (Basios 2025).

Aneurysm Formation

Aneurysmal disease is mediated by proteolytic degradation of elastin and collagen in the aortic wall, upregulation of matrix metalloproteinases, chronic inflammation, and biomechanical stress. Abdominal aortic aneurysm (AAA) is associated with infiltration of T cells and macrophages, while TAA often relates to genetic mutations affecting connective tissue proteins such as fibrillin (Sakalihasan 2018).

Thrombosis

Arterial thrombosis is platelet-driven, while venous thrombosis is fibrin-rich. Both involve the coagulation cascade and interplay between clotting factors and endothelium. Atrial fibrillation (AF) is a major source of systemic arterial thromboembolism, where stasis, particularly in the left atrial appendage, leads to thrombus formation (Writing Committee 2022). Pulmonary embolism (PE) arises from embolization of venous thrombi (Rutherford 2018).

Venous Insufficiency

Venous reflux increases hydrostatic pressure, leading to capillary leak, leukocyte trapping, inflammation, and tissue damage. This cascade underlies chronic venous ulcers (Greenhalgh 2010)📄. Management of chronic venous insufficiency (CVI) and associated lymphedema often involves compression therapy; non-pneumatic compression (NPC) has been recognized for its clinical utility in managing these conditions (Jacobowitz 2025). For refractory venous ulcers, platelet-rich plasma (PRP) has shown clinical efficacy in improving healing rates and outcomes (Rodrigues 2026).

Diagnostics and Imaging

Diagnosis integrates history, physical examination, hemodynamic testing, and imaging.

Clinical Assessment

History of claudication, rest pain, ulceration, or embolic events is essential. On examination:

• Arterial: pulse deficit, bruits, trophic skin changes. In patients with diabetes, a comprehensive foot examination is mandatory to identify neuropathy, deformity, and skin integrity issues (Das 2025).
• Venous: varicosities, edema, skin pigmentation, ulceration.
• Lymphatic: swelling, non-pitting edema, skin thickening.

For peripheral artery disease (PAD), risk-stratify limb threat with Wound, Ischemia, and foot Infection (WIfI) staging and integrate with patient risk, limb threat, and anatomic pattern (PLAN) to guide revascularization strategy (Conte 2019)📄. Angiographic scoring systems within the PLAN framework are increasingly utilized to predict clinical outcomes and technical success (Lyons 2026).

Perioperative Cardiac Risk Assessment

Vascular surgery patients have high rates of coronary artery disease. The Revised Cardiac Risk Index (RCRI) helps stratify perioperative major adverse cardiac events (MACE) risk before non-cardiac surgery (Lee 1999)📄. Vascular procedures (especially aortic and lower extremity) are classified as high-risk surgery, contributing 1 point to the RCRI score. In patients with established atherosclerotic cardiovascular disease (ASCVD), the SMART2-HF model may be used to predict the risk of incident heart failure, further refining the clinical profile of the high-risk vascular patient (Reitsma 2026).

Hemodynamic Testing

• ankle-brachial index (ABI): Sensitivity ~80%, specificity ~95% for peripheral arterial disease (PAD) (Aboyans 2012)📄. Limitations: falsely elevated in calcified arteries.
• toe-brachial index (TBI): Preferred over ABI in patients with diabetes or chronic kidney disease (CKD) due to medial arterial calcification and non-compressible vessels (Potier 2011)📄^,(Das 2025).
• transcutaneous oxygen tension (TcPO₂): Values <30 mmHg indicate severe ischemia with poor wound-healing potential; 30–39 mmHg suggests moderate ischemia; ≥40 mmHg indicates adequate perfusion (Schepers 2010)📄.
• Segmental pressures and plethysmography: Localize stenoses and assess venous reflux.

In chronic limb-threatening ischemia (CLTI), toe pressure <30 mmHg or TcPO₂ <30 mmHg indicates severe ischemia and poor wound-healing potential. The Wound, Ischemia, and foot Infection (WIfI) staging system integrates hemodynamics (toe pressure, TcPO₂), wound characteristics, and infection severity to stratify limb threat and guide revascularization decisions (Conte 2019)📄^,(Das 2025). See 10Ch. 10 for complete WIfI classification.

Imaging Modalities

• Duplex Ultrasound (DUS): First-line for peripheral arterial disease (PAD), abdominal aortic aneurysm (AAA), carotid stenosis, venous reflux, and deep vein thrombosis (DVT). Operator-dependent but safe and inexpensive (Moneta 2010)📄. In patients with diabetes, DUS is the preferred initial imaging modality for PAD (Das 2025).
• computed tomography angiography (CTA): Provides high-resolution 3D reconstructions for aneurysms and PAD; requires contrast and radiation (Sun 2011)📄. CTA is highly effective for identifying the multi-segmental and infrapopliteal disease patterns common in diabetic patients (Das 2025).
• magnetic resonance angiography (MRA): Useful when CTA contraindicated; gadolinium-based contrast or time-of-flight techniques (Prince 2016). MRA is an alternative for detailed anatomical assessment in PAD, particularly when avoiding ionizing radiation is prioritized (Das 2025).
• Catheter angiography: Remains the gold standard; allows simultaneous diagnosis and treatment but carries procedural risk (White 2006)📄.
• intravascular ultrasound (IVUS) and optical coherence tomography (OCT): Provide intraluminal detail; OCT superior for plaque characterization, IVUS for stent sizing (Ali 2016).
• positron emission tomography/computed tomography (PET/CT): Detects active inflammation in aneurysm walls and vulnerable plaques (Figueroa 2015)📄.

Medical Management

• Lifestyle modification: Smoking cessation reduces abdominal aortic aneurysm (AAA) expansion and peripheral arterial disease (PAD) progression (Golledge 2017)📄. Exercise therapy improves walking distance in PAD. Comprehensive risk factor modification, including diet and physical activity, remains the cornerstone of cardiovascular prevention (Al 2025).
• Antiplatelet therapy: Aspirin or clopidogrel for secondary prevention in symptomatic atherosclerotic disease (CAPRIE 1996).
• Anticoagulation: Low-dose rivaroxaban plus aspirin benefits select PAD patients; see 10Ch. 10 for COMPASS/VOYAGER-PAD evidence and patient selection criteria.
• Lipid lowering: High-intensity statins reduce events and slow aneurysm growth (Al 2025). Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors provide additional risk reduction in statin-intolerant or high-risk patients (Sabatine 2017)📄.
• Blood pressure and glycemic control: Angiotensin-converting enzyme (ACE) inhibitors and tight glycemic control improve vascular outcomes (Patel 2016)📄. In patients with diabetes and PAD, management requires intensive risk factor control and the use of evidence-based glucose-lowering therapies to reduce the risk of major adverse limb and cardiovascular events (Das 2025).
• Risk stratification: In patients with established atherosclerotic cardiovascular disease (ASCVD), the SMART2-HF model can be utilized to predict the risk of incident heart failure, facilitating early intervention and personalized management (Reitsma 2026).

Open Surgery

• Bypass grafting: Autologous vein remains gold standard for infrainguinal bypass (Conte 2018)📄. See 10Ch. 10 for BEST-critical limb ischemia (CLI)/BASIL evidence.
• carotid endarterectomy (CEA): Standard for symptomatic carotid stenosis >50% and select asymptomatic stenosis >70%. See 7Ch. 7 for NASCET, CREST, and patient selection.
• Open abdominal aortic aneurysm (AAA) repair: Durable long-term results, particularly for young/fit patients (Lederle 2002). See 4Ch. 4.
• Thrombectomy/Embolectomy: Fogarty embolectomy remains the standard for acute embolic occlusion (Rutherford 2018).

> See Also: Disease-specific surgical details: 4Ch. 4, 7Ch. 7, 10Ch. 10.

Endovascular Therapy

• percutaneous transluminal angioplasty (PTA): Widely used for focal lesions, especially in iliac arteries.
• Drug-coated devices: Drug-coated balloons (DCB) and drug-eluting stents (DES) improve patency in femoropopliteal disease; see 10Ch. 10 for evidence and paclitaxel safety considerations.
• endovascular aneurysm repair (EVAR)/thoracic endovascular aortic repair (TEVAR): Reduced perioperative mortality compared to open repair; see 4Ch. 4 for RCT evidence and patient selection.
• Thrombectomy: Penumbra Indigo and AngioJet systems effective in acute limb ischemia (ALI) (Hsiao 2019).
• Embolization: Indicated for visceral aneurysms, endoleaks, and hemorrhage control, including arterial embolization for hemodynamically unstable pelvic fractures (Anand 2022).
• resuscitative endovascular balloon occlusion of the aorta (REBOA): Utilized for temporary hemorrhage control in trauma patients with life-threatening subdiaphragmatic bleeding, often as part of a multi-modal approach alongside angioembolization or surgery (Anand 2022).

> See Also: Disease-specific techniques: 4Ch. 4, 10Ch. 10, 16Ch. 16.

Hybrid Approaches

Hybrid approaches combine open and endovascular methods, such as iliac stenting with femoral thromboendarterectomy (TEA) or visceral debranching with thoracic endovascular aortic repair (TEVAR), offering flexibility for complex anatomy (Bisdas 2013)📄. These strategies are increasingly utilized in the management of acute and chronic mesenteric ischemia, particularly for complex lesions requiring combined access (Alonso 2025). Furthermore, long-term registry data support hybrid repair as a durable treatment modality for extracranial carotid artery aneurysms (ECAA) (Willemsen 2025).

Table 1.2. Comparison of Treatment Options

Follow-up

Surveillance ensures early detection of complications such as graft stenosis, endoleaks, and restenosis.

• endovascular aneurysm repair (EVAR): computed tomography angiography (CTA) or duplex ultrasound (DUS) at 1 month, 12 months, then annually (European Society for Vascular Surgery (ESVS), Society for Vascular Surgery (SVS)) (Aburahma 2019)📄.
• Open abdominal aortic aneurysm (AAA) repair: Imaging only if symptomatic.
• Bypass grafting: DUS at 1–3, 6, 12 months, then annually (Almasri 2018)📄.
• Carotid (carotid endarterectomy (CEA)/carotid artery stenting (CAS)): DUS at 6 months, then every 1–2 years (Naylor 2018)📄.
• Venous intervention: DUS at 1–3 months, then as clinically indicated.

For EVAR, risk-stratified surveillance per ESVS AAA guidance suggests that many standard EVARs may transition to duplex-based annual follow-up after a stable first-year scan, while complex anatomies or endoleaks require individualized schedules (ESVS 2024)^,(Aburahma 2019)📄. Recent multicenter data supports the implementation of these updated algorithms, highlighting that 1-year sac dynamics (specifically sac shrinkage) are critical for predicting long-term stability and further refining the intensity of follow-up (Esposito 2025).

Surveillance Intervals

Table 1.3. Recommended Surveillance Intervals by Procedure

Carotid surveillance per 7Ch. 7: DUS at 1, 6, and 12 months, then annually; adjust based on residual stenosis, periprocedural complications, or contralateral disease (Tessarek 2023).

Foundational vascular anatomy and hemodynamics

The vascular system is organized into distinct anatomic territories, each with characteristic arterial, venous, and lymphatic components. Arterial anatomy includes the cervical and cerebrovascular territories, the thoracic aorta with its arch zones (0–3), the visceral and mesenteric circulation, the iliofemoral system, and the below-knee angiosomes. Key collateral networks include the circle of Willis for cerebral perfusion, the marginal artery of Drummond and arc of Riolan for mesenteric collateralization, and the genicular network around the knee.

Venous anatomy comprises the deep, superficial, and perforator systems, with the calf-muscle pump playing a central role in venous return. The lymphatic channels parallel the vascular tree and drain into regional lymph nodes.

Angiosome-directed revascularization refers to restoring blood flow to specific tissue zones based on direct arterial supply. In chronic limb-threatening ischemia (CLTI), this approach may improve wound healing outcomes, though evidence remains evolving (Conte 2019)📄. Standard vascular nomenclature includes aortic arch zones (0–3), femoropopliteal segments, and named tibial vessels (anterior tibial, posterior tibial, and peroneal arteries).