Take-home messages

1. The comorbidity HF and stroke is a high-risk condition that requires interdisciplinary efforts including cardiologist expertise in diagnostic workup, monitoring of complications and initiation of secondary prevention.
2. The interaction between stroke and HF is bidirectional: HF can induce stroke, and stroke can induce or worsen HF.
3. The highest risk of stroke occurs within the first 30 days of new HF diagnosis - avoiding acute HF decompensation is highly effective to reduce the risk of stroke.

Abbreviations

AF: atrial fibrillation

ADHF: acute decompensated heart failure

BP: blood pressure

ESC: European Society of Cardiology 

HF: heart failure

HFpEF: heart failure with preserved ejection fraction

HFrEF: heart failure with reduced ejection fraction

Keywords  

cardiac reflex, cognition, heart failure, mood, muscle, stroke

Disclaimer

This paper is a condensed version of the clinical consensus statement on heart failure and stroke interaction of the ESC Council on Stroke, the Heart Failure Association and the ESC Working Group on Thrombosis [1].

Introduction and epidemiology

Heart failure (HF) and stroke are two major cardiovascular conditions that frequently coexist, leading to significant morbidity and mortality. Stroke and HF share common risk factors such as hypertension, diabetes, and atherosclerosis, and they are mechanistically interconnected through thromboembolic activation, haemodynamic failure, and neuroendocrine dysregulation. Notably, the interaction between stroke and HF is bidirectional, which means that HF is a risk factor for stroke through thromboembolism and impaired cardiac output, while in turn, stroke is a risk factor to induce or worsen HF and acute decompensation of HF by disrupting autonomic cardiovascular regulation (Figure 1) [2]. These interrelations have been conceptualised as the "cardio-cerebral syndrome" (HF-induced brain injury [3]) and "stroke-heart syndrome" (stroke-induced myocardial dysfunction) [4].

Figure 1. Bidirectional interaction of heart failure and stroke. Reproduced with permission from [1].

AF: atrial fibrillation; BP: blood pressure; CHF: congestive heart failure; HF: heart failure; LV: left ventricule

Stroke affects approximately 100 million people worldwide, accounting for over 6.6 million deaths annually. It remains a leading cause of adult disability, particularly in Europe. Similarly, HF affects 1–2% of the adult population in developed nations, with prevalence rising significantly in older populations.  HF is present in 10–24% of ischaemic stroke patients, either as a pre-existing condition or with onset triggered by the stroke itself as stress-induced cardiomyopathy. Echocardiographic data indicate that 10% of stroke patients have systolic HF, while 23% exhibit diastolic dysfunction [5]. HF patients with stroke also tend to have more advanced comorbidity profiles with higher rates of diabetes, coronary artery disease, and atrial fibrillation (AF), all of which further increase the risk of recurrent stroke and cardiovascular events.

Conversely, HF patients exhibit an elevated risk of ischaemic stroke. Clinical studies and registries report a stroke prevalence of 8–11% in HF patients. A clinically important observation is that the highest stroke risk occurs within the first 30 days after

HF, with a 5- to 17-fold increase in different studies [6]. Additionally, HF patients in sinus rhythm still carry a heightened stroke risk compared to non-HF individuals, with AF further compounding this risk. Notably, recent evidence suggests that stroke risk is comparable or even higher in patients with HF with preserved ejection fraction (HFpEF) than in those with reduced ejection fraction (HFrEF), likely due to comorbidities and advanced age.

Stroke outcomes are markedly worse in patients with comorbid HF: in these patients the cerebral infarction is often larger and is associated with higher mortality and greater long-term disability. Cardioembolic stroke is the predominant aetiology of stroke in HF, which often leads to multiterritorial infarcts or proximal artery occlusion with larger territories affected and more severe neurological deficits. Stroke recurrence is also significantly higher, and mortality rates post-stroke are up to 4.5 times greater in HF patients. Functional recovery is poor, with a 2- to 3-fold increased risk of severe disability (modified Rankin scale 3–6). The COMMANDER HF trial reported that nearly half of all strokes in HF patients were either fatal or disabling [7].

Given these challenges, optimal management of the HF-stroke comorbidity requires a multidisciplinary approach with contributions needed from cardiologists for diagnostic workup, monitoring of cardiovascular complications in the acute and subacute phase of stroke (i.e. stroke unit care) and to initiate long-term treatment for cardiovascular comorbidities. The role of oral anticoagulation in HF for stroke prevention remains a topic of ongoing research, with emerging evidence suggesting potential benefits beyond AF-related risk. Early intervention, close monitoring in stroke units, and tailored therapeutic strategies are essential to mitigate adverse outcomes.

Mechanisms of interaction of heart failure and stroke 

Mechanisms of heart failure leading to stroke

Cardioembolism is the most common aetiology of stroke in HF but other aetiologies (macrovascular stroke, microvascular strokes, PFO associated, rare causes) also apply. A number of mechanisms contribute to the increased stroke risk in HF patients with the Virchow triad of thrombus formation being activated in all three components [8]:

• a hypercoagulable state with activation of multiple prothrombotic factors,
• endothelium dysfunction to support thrombus formation and adhesion,
• blood stasis and abnormal blood flow.

Further HF-related factors include:

• reduced cardiac output and cerebral hypoperfusion,
• atrial fibrillation, which is a common comorbidity in HF,
• neurohormonal dysregulation in HF which exacerbates systemic inflammation and prothrombotic states.

HF-related stroke risk is particularly high in acute decompensated heart failure (ADHF), where transient hypotension and hypoperfusion exacerbate cerebral ischaemia. In chronic HF, persistent low-grade inflammation and endothelial dysfunction sustain the heightened stroke risk. Moreover, HF patients in sinus rhythm remain at elevated stroke risk due to left atrial enlargement and fibrosis.

Mechanisms of stroke leading to or aggravating heart failure

Stroke can induce acute and chronic cardiac dysfunction, collectively termed "stroke-heart syndrome" [4]. Sympathetic overactivation following acute stroke results in catecholamine surges, leading to myocardial stunning, arrhythmias, and Takotsubo-like cardiomyopathy. Ischaemic stroke, particularly involving the insular cortex, disrupts autonomic control, causing haemodynamic instability, increased myocardial oxygen demand, and potential cardiac decompensation (Figure 2).

Figure 2. Signalling pathways in acute and subacute stroke to provoke cardiac injury and to induce or aggravate heart failure. Reproduced with permission from [1].

HF: heart failure

Stroke patients with preexisting HF are at higher risk for ADHF due to volume overload, hypertension, and stress-induced myocardial dysfunction. In patients without prior HF, stroke-induced myocardial injury may lead to new-onset HF, particularly in those with underlying ischaemic heart disease or diastolic dysfunction.

Notably, the severity of the autonomic dysfunction and resulting myocardial injury are associated with injury of certain cerebral regions (including the insula region, the anterior cingulate gyrus, and the amygdala) [9]. Stroke-related cardiac changes are usually transient within the subacute phase of 2 to 5 days [10].

What are the risk factors of stroke in HF patients

The stroke risk of patients with HF depends on clinical variables of the HF plus additional patient-specific characteristics and comorbidities (Table 1). As pointed out above, a temporal association of a particularly high stroke risk early after a de novo diagnosis of HF (<30 days) applies. In addition to this early high risk, the risk of stroke in these patients accumulates over time, reaching 1.4% after one year, 2.9% after three years, and 3.9% after five years [11].

Table 1. Clinical parameters which are known to affect the stroke risk in HF patients.

HF: heart failure

The main factors that increase the risk of stroke in HF are:

• age, which plays a crucial role, as both heart failure and stroke are more prevalent in older patients;
• myocardial factors such as impaired contractility, enlarged atrial and ventricular volumes, and reduced cardiac blood flow contribute to thrombogenesis. Interestingly, while reduced left ventricular systolic function alone does not appear to be a dominant risk factor, an elevated E/e’ ratio and increased NT-proBNP levels are predictive of higher stroke risk.
• AF is a major cause of stroke and is reciprocally linked with heart failure. Patients with both HF and AF have a worse prognosis and a higher stroke risk than those in sinus rhythm. Notably, patients with paroxysmal AF in HF studies exhibit a greater stroke risk than those with persistent or permanent AF. Even in the absence of AF, the CHA2DS2-VASc score can serve as a valuable risk stratification tool in patients with HF [12]. Studies indicate that HF patients with an extensive risk profile yet without AF have a stroke risk equivalent to that of non-anticoagulated AF patients;
• left ventricular (LV) thrombus may occur in HF patients particularly in connection to LV regional akinetic segments or aneurysms and has an obvious mechanistic association with ischaemic stroke. Patients with left ventricular thrombus have a 9% short-term risk of stroke [13] and should be considered for oral anticoagulation [14].

Additional comorbidities such as diabetes mellitus, chronic kidney disease, and inflammatory disorders further elevate the risk. Diseases with systemic inflammation and venous vascular diseases may exacerbate thromboembolic risk. Given the complexity of these risk factors, individualised risk stratification and cardiologic expertise in interdisciplinary treatment are essential to minimising cardiovascular risk.

Stroke prevention and anticoagulation strategies in heart failure

Stroke prevention is crucial in reducing the global burden of stroke, with up to 90% of strokes considered preventable through management of modifiable risk factors. In HF, primary and secondary stroke prevention follows similar principles as in non-HF patients, focusing on controlling cardiovascular and cerebrovascular risk factors, including hypertension, AF, atherosclerotic disease, lipid disorders, and lifestyle factors such as smoking, alcohol use, physical inactivity, and obesity. Other risk factors, like diabetes, sleep-disordered breathing, and a family history of stroke or AF also contribute to increased risk. Once HF is diagnosed, however, stroke risk increases, necessitating further diagnostic workups and continuous monitoring. An echocardiographic evaluation of the left atrium and ventricle is essential in assessing and managing stroke risk.

Primary and secondary stroke prevention in heart failure

Preventing stroke in HF patients is rooted in optimising heart failure treatment according to clinical guidelines [14]. Preventing acute decompensated heart failure (ADHF) can significantly reduce stroke risk. If decompensation of HF occurred, treatment for recompensation should take into account the heightened stroke risk and should apply careful management and monitoring, in particular no brisk volume rebalancing, and preventing infections.

Primary prevention requires managing risk factors such as AF, atherosclerosis, hypertension, and diabetes. As AF is closely linked with both HF and stroke, timely detection and treatment of AF are vital for stroke prevention. Screening for AF is recommended for elderly patients (≥65 years) and systematically in those aged ≥75 years. Patients with device-detected rhythm abnormalities should be further evaluated, as AF may be subclinical. Anticoagulation therapy is critical in AF management to prevent strokes in both HF and non-HF patients.

Secondary prevention in stroke patients requires a thorough cardiac evaluation, especially if symptoms or family history suggest a cardiac cause for the stroke. A common clinical situation is that an acute stroke brings a patient to the hospital and the diagnostic workup reveals a hitherto undetected cardiac disease (including HF) to underly the stroke. Monitoring for AF burden [15] and evaluating the option for AF ablation should be pursued to improve outcome in patients with HF [16]. The CHA2DS2-VASc (or the new CHA2DS2-VA)- score helps in stratifying stroke risk and guiding anticoagulation therapy.

Oral anticoagulation for stroke prevention in heart failure

Oral anticoagulation is key to prevent cardioembolic stroke in HF patients, especially in those with AF. The European Society of Cardiology (ESC) guidelines clearly recommend oral anticoagulants (OACs) for HF patients with AF preferably with direct oral anticoagulants (DOACs). Randomised controlled trials (RCTs) have shown that DOACs reduce recurrent stroke risk by 64% and all-cause mortality by 26%, supporting their use for stroke prevention.

In patients with HF but no AF, the benefit of anticoagulation for stroke prevention is less clear. RCTs such as the WARCEF trial found no significant benefit of warfarin over aspirin in preventing stroke or death in HF patients with sinus rhythm. The reduced ischaemic stroke rates using warfarin were offset by increased major bleeding risks. The COMMANDER HF trial, which studied rivaroxaban in HF patients with sinus rhythm, found no significant difference in major adverse cardiovascular event (MACE) endpoints (death, myocardial infarction, or stroke). A post hoc analysis showed a 32% reduction in ischaemic strokes, but this benefit was offset by more major bleeding events. A meta-analysis also found a reduction in stroke or systemic embolism, but with an increased rate of major bleeding.

For HF patients with preserved or mildly reduced ejection fraction, low-dose rivaroxaban may be considered if there is comorbid coronary artery disease or peripheral artery disease, as it reduces ischaemic events. However, anticoagulation should be avoided in patients at high bleeding risk, and alternative methods like left atrial appendage closure (LAAC) may be considered. LAAC has proven effective for stroke prevention in AF patients with HF, with observational data showing no difference in in-patient mortality or cardiac complications between HF and non-HF patients [17].

Specific aspects of HF treatment after stroke

The management of HF after a stroke should follow the current HF management guidelines taking into account the different recommendations for HFrEF and HFpEF [14]. In the vulnerable phase after stroke, maintaining cardiac output, normal blood pressure, heart rate and heart rhythm are crucially important for both improving outcome after stroke and preventing episodes of ADHF.

Whenever possible, ongoing HF therapy should be continued. However, temporary dose reductions may be needed, as many HF drugs lower blood pressure (BP). Even without clinical hypotension, excessive BP reduction can compromise cerebral perfusion. Special care is required with beta-blockers, which should never be abruptly discontinued due to the risk of rebound sympathetic activation, arrhythmias, and sudden cardiac death. In the post-acute phase, re-initiation and up-titration of HF medications to target doses are crucial. Besides reducing HF-related morbidity and mortality, they also serve a secondary preventive role by lowering BP. Ideally, full HF therapy should be re-established before adding further antihypertensive agents.

BP control can be particularly challenging in HF patients after stroke. The relationship between systolic BP and mortality follows a J- or U-shaped curve, with optimal outcomes in the 130–150 mmHg range. Acute stroke may trigger transient hypertension due to autonomic dysregulation, which increases the risk of cerebral oedema, haemorrhagic transformation, but also HF deterioration. Conversely, HF-related hypotension may impair cerebral perfusion and promote border-zone (watershed) infarcts. Thus, extreme BP values should be avoided, and BP-lowering strategies must be cautiously and individually reintroduced after the acute phase. Additionally, sympathetic activation after stroke can lead to tachycardia or new-onset AF, which may aggravate HF. In such cases, (re-) introduction or up-titration of beta-blockers is beneficial, and ivabradine may be considered in patients with sinus rhythm and persistent tachycardia.

Specific aspects of acute stroke treatment in HF patients

Reduced cardiac output has been observed in up to 25% of patients in acute stroke, making adequate cerebral perfusion especially difficult in the context of pre-existing HF. Notably, cerebrovascular autoregulation is impaired during acute stroke, therefore in this phase, cerebral blood flow becomes directly dependent on systemic cardiac output. In patients with low ejection fraction and hypotension, this increases the risk of border-zone infarction. Carefully balanced fluid administration can help restore perfusion pressure but must be used cautiously to avoid volume overload and ADHF.

In haemorrhagic stroke, by contrast, prompt BP reduction is essential to limit haematoma expansion and reduce cardiac strain from acute hypertensive episodes. BP targets must be personalised, considering the stroke type, baseline BP, cardiac function, and the use of thrombolysis. Evidence for reperfusion therapies in HF patients is limited. Although HF patients were largely excluded from clinical trials, retrospective analyses suggest similar efficacy and safety of thrombolysis and thrombectomy compared to non-HF patients. However, HF may be associated with poorer collateral circulation and greater anaesthetic complexity during interventions, which could influence outcomes.

The coexistence of HF and stroke requires a tailored therapeutic approach that balances cerebral and cardiac needs. Guideline-directed therapies should be maintained where possible, with careful haemodynamic monitoring and individualised adjustments throughout the acute and subacute phase after stroke.

Cardiac complications and heart failure management in the stroke unit

Stroke unit care significantly improves both short- and long-term outcomes after an acute stroke, including mortality reduction and increased independence, largely due to multidisciplinary management and proactive control of complications. Cardiac complications—such as HF, myocardial infarction, Takotsubo cardiomyopathy, arrhythmias, and acute hypertensive episodes—are common, especially within the first 72 hours post-stroke (see stroke-heart syndrome, above), and are linked to poor prognosis [18].

HF patients are particularly vulnerable to acute cardiac complications. Pre-existing cardiac dysfunction increases susceptibility to neurogenic cardiac injury, raising the risk of complications and contributing to worse outcomes. Stroke unit care should therefore include systematic attendance by an experienced cardiologist. Three priorities should be addressed in the cardiac care during stroke unit treatment: a) support the diagnostic workup to identify the stroke aetiology (cardiovascular aetiology is common), b) support and advise on cardiovascular monitoring findings to prevent cardiac complications, and c) initiating secondary prevention strategies including optimised HF management which may be continued after the stroke unit care.

Monitoring strategies include electrocardiogram (ECG) for arrhythmia detection, especially AF, which occurs in up to 10% of stroke patients. Fluid balance, blood pressure control, cardiac biomarker monitoring (natriuretic peptides and high-sensitive troponin (hs-cTn) to support clinical evaluation), and cardiac imaging are also important. Repolarisation changes on ECG occur early and may be a sign of arrhythmic risk and higher mortality.

Elevated hs-cTn is frequently observed, even without acute coronary syndrome. Notably, only about 25% of patients with dynamic hs-cTn elevations have a culprit lesion that would benefit from a coronary intervention.

While direct evidence for the efficacy of stroke unit care in HF patients is limited, their haemodynamic vulnerability and high complication risk support the need for structured, cardiology-integrated stroke unit care.

Cerebral complications including stroke and cognitive decline in acute heart failure

Acute decompensated heart failure poses a significant risk for cerebral complications, particularly ischaemic stroke and cognitive decline. Between 6.5% and 15% of all strokes occur during hospitalisation, with cardiac disorders being a major reason for the index hospitalisation. Even in the absence of AF, patients with acute HF are at high stroke risk, both during the hospitalisation for acute HF and shortly after discharge.  Risk prediction tools like the CHA₂DS₂-VASc score are applicable (even in HF patients without AF). Pre-existing cerebrovascular disease worsens outcomes in ADHF. The ASCEND-HF trial showed an 80% increase in death or rehospitalisation risk in patients with such a history [19].

Pathophysiologically, ADHF creates a pro-thrombotic state through low cardiac output, endothelial dysfunction, systemic inflammation, neurohormonal activation, and haemodynamic changes—heightening stroke risk, particularly in early stages of HF diagnosis. Cardioembolism accounts for about 64% of strokes in ADHF, especially in patients with high natriuretic peptides or newly diagnosed HF. The VALIANT trial showed stroke risk rises with ventricular dysfunction severity [20]. HF itself also worsens outcomes post-stroke, contributing to a vicious cycle of mutual deterioration. Stroke risk differs by HF phenotype. Data from over 2.5 million U.S. patients show higher stroke incidence in acute HF with reduced (4.1%) versus preserved ejection fraction (2.5%) [21].

Beyond stroke, acute HF is associated with cognitive impairment and depression. Cognitive deficits may partially reverse post-recompensation, while silent infarctions and depression are common. Depression affects 20–50% of HF patients and worsens outcomes. Although selective serotonin reuptake inhibitors are safe, they don’t improve prognosis; tricyclics should be avoided due to cardiovascular risks.  In summary, acute HF is a high-risk condition for patients to suffer stroke and neuropsychiatric complications. Integrated cardiology-neurology care, early brain imaging, careful haemodynamic management, and attention to cognitive and psychological status are essential to improve outcomes.

Summary and consensus statements

The comorbidity of HF and stroke represents a high-risk condition. The comprehensive care of stroke patients benefits largely from interdisciplinary involvement of cardiologist’ expertise in diagnostic workup, close subacute monitoring of complications and initiation of long-term secondary prevention and cardiovascular treatment in patients with newly diagnosed cardiovascular diseases.

The main consensus statements on HF-stroke interaction are:

Epidemiology

• Stroke occurs in 8–11% of HF patients, especially in the first 30 days or during ADHF episodes.
• Risk factors include age, HF duration/severity, and comorbid atrial fibrillation (AF).
• Up to 24% of acute ischaemic stroke patients have HF, either pre-existing or newly developed in the acute stroke phase, with worse outcomes than those without HF.

Mechanisms

• Cardioembolism is the main cause of stroke in HF (~40–50%), with hypoperfusion and vascular disease also contributing.
• HF activates all components of Virchow’s triad, increasing the thromboembolic risk.
• Stroke, in turn, can induce cardiac complications (“stroke-heart syndrome”), including arrhythmias and acute HF.
• Low cardiac output reduces cerebral perfusion, worsening ischaemic injury.

Diagnostic workup

• Cardiac history, ECG, and transthoracic echocardiography are essential.
• Biomarkers help assess myocardial injury and guide treatment decisions in the subacute stroke phase.

Treatment & prevention

• Preventing decompensation in HF is critical to avoid strokes.
• Anticoagulation is indicated in patients with AF but needs individual evaluation in patients with sinus rhythm.
• Stroke units should manage all acute stroke patients, including those with HF.
• HF medications (e.g., angiotensin-converting enzyme [ACE] inhibitors, angiontensin receptor neprilysin inhibitor [ARNI], sodium-glucose cotransporter-2 [SGLT2] inhibitors, beta-blockers) should be maintained or resumed early.
• Cardiologists should routinely be involved in the stroke unit care.
• Long-term HF and cardiovascular management should continue post-discharge, with individualised coronary diagnostics as needed.