Stroke patients have an increased risk of death resulting from myocardial infarction when compared to the general population [8], with cardiovascular disease being the most common cause of death in 1-year stroke survivors [9]. A substantial amount of stroke patients have asymptomatic coronary stenosis, thus indicating coronary artery disease [10]. Despite this known increased risk and, indeed, the presence of asymptomatic coronary artery disease, systematic evaluation of asymptomatic patients with coronary artery disease in the form of coronary angiography is not currently recommended following a recent ischaemic stroke. This, in part, may have resulted from safety concerns regarding coronary angiography in stroke patients and relates to the increased risk of brain haemorrhagic transformation and parenchymal haemorrhage secondary to anticoagulation therapy during the procedure. In a study published in 2010 in which coronary angiography was conducted to show previously unknown coronary artery disease in a large cohort of patients with ischaemic stroke, coronary angiography proved to be safe even 6–11 days post-stroke (acute phase), with only 1 adverse procedural event (groin haematoma), in the 315 patients who underwent coronary angiography [10]. Nonetheless, whether stroke patients with asymptomatic coronary artery disease should be investigated with coronary angiography as a matter of routine continues to be debated. A meta-analysis of 39 studies which included 65,996 patients with a mean follow-up of 3.5 years post-acute stroke or transient ischaemic attack, revealed the annual risk of both myocardial infarction and non-stroke vascular death to be approximately 2 %. The accumulation of risk was linear, with the risk of myocardial infarction 10 years after acute stroke being approximately 20 % [11]. Additionally, stroke of carotid origin is viewed as a coronary heart disease risk equivalent implying that this should hold true to stroke patients without carotid artery disease or without coronary artery disease [12].

There are a number of mechanisms through which acute stroke may induce myocardial injury. These include catecholamine-induced cardiac dysfunction, whereby neurohumoral changes post-stroke can contribute to cell death, coronary artery vasospasm, and cardiac arrhythmias [1, 13, 14]. Indeed, stroke affecting the insular cortical area, which is involved in normal cardiac autonomic regulation, has been associated with adverse cardiac events including myocardial infarction [14]. This implies neurogenic cardiac damage due to autonomic activation after acute ischaemic stroke as a potential mechanism. Interestingly, there is now greater focus on the association between specific markers of myocardial injury and acute stroke and whether examining the levels of cardiac muscle regulatory protein troponin T (cTnT) can lend support to the different pathophysiological mechanisms of myocardial injury and subsequent diagnostic cardiac work up [10]. Increased levels of troponin are seen in between 5 and 34 % of patients with acute ischaemic stroke, and there is an association between elevated levels and stroke severity, cardiovascular abnormalities (including left ventricular dysfunction, hypotension, and pulmonary oedema), right insular cortical involvement, and unfavourable short- and long-term outcomes [15]. The main causes of elevated troponin levels in the absence of renal dysfunction are twofold. Acute coronary syndrome in association with acute stroke caused by coronary vascular occlusion leading to myocardial necrosis is one mechanism, but the prevalence of this event using coronary angiography is limited [10]. Secondly, cerebral autonomic dysregulation with subsequent catecholamine surge leading to myocardial injury and ventricular dysfunction is an increasingly recognised phenomenon [14]. Whether coronary angiography should be implemented in patients with elevated Troponin levels is unclear, and such intervention needs to be carefully balanced with the risks of the procedure and subsequent therapeutic intervention such as dual antiplatelet and anticoagulation therapy. Clearly, careful risk stratification is important in identifying patients who are at high risk of cardiac events, and these may include patients with previous cardiac events, diabetes, peripheral vascular disease, atrial fibrillation, and large-vessel strokes. How best to investigate these patients however, and the timing of such intervention, requires clarification [16].

The prevalence of chronic heart failure increases with age, with 1–2 % of adults in developed countries living with a chronic heart failure diagnosis. In those over 80 years old, one in ten adults have chronic heart failure, and those aged over 40 have a lifetime prevalence of one in five [17, 18]. Studies have indicated that the risk of ischaemic stroke is two to three times higher for patients with chronic heart failure than it is for patients without chronic heart failure [19, 20]. In fact, epidemiological data suggest that between 10 and 24 % of patients with stroke have evidence of congestive heart failure, and that the stroke risk is highest within the first month after diagnosis of heart failure but normalises within 6 months [21–24]. It is therefore unsurprising that prospective studies have demonstrated that the annual stroke rate is increased in patients with congestive cardiac failure and concomitant atrial fibrillation, with annual stroke rates described between 10 and 16 % [25]. Moreover, there is reportedly a 9–10 % risk of recurrent stroke per year in stroke patients with chronic heart failure [26].

There are a number of mechanisms that contribute to stroke in patients with chronic heart failure. These include thrombus formation secondary to left ventricular hypokinesia, reduced ejection fraction and atrial fibrillation, increased coagulation (D Dimer and thrombin concentration), increased endothelial cell activation and damage, in addition to both large- and small-vessel cerebrovascular disease with their association with both hypertension and diabetes [27].

Patients with congestive heart failure have higher mortality associated with stroke, with one study depicting a doubling risk of death (OR: 2.3; 95 % CI, 1.8–2.9) [20]. In addition, patients with congestive heart failure have more severe neurological deficits and longer hospital stays than those without heart failure [24]. Of note, acute coronary syndrome, arrhythmia, excessive fluid hydration, and poor or non-compliance with medication can precipitate a worsening of heart failure in high-risk patients. There is also increasing evidence of an association between the severity of cardiac dysfunction and cerebral ischaemic lesions described on MR findings giving rise to “silent strokes” [28]. These features may be exhibited by alterations in neuropsychological function including decreased attention, memory loss, and concentration deficits [29], occurring as a consequence of impaired cerebrovascular reactivity. The Rotterdam Scan Study demonstrated that these “silent strokes” on MR imaging occurred in approximately 20 % of patients aged between 60 and 90 years with congestive heart failure [30].

Echocardiographic wall motion abnormalities have also been described in patients with both ischaemic and haemorrhagic stroke as a result of disturbance in autonomic central control, resulting in excessive catecholamine release. Left apical ballooning and subsequent left ventricular dysfunction, leading to a unique kind of cardiomyopathy termed Takotsubo syndrome, has been described [31]. This syndrome is associated with impaired apical ventricular contraction, resulting in an increased risk of sudden death, congestive heart failure, and arterial thrombus formation. This syndrome is seen in patients with elevated troponin levels in the absence of obstructive coronary artery disease and is associated with temporary ST elevation followed by significant T wave inversion in the anteroseptal leads on a 12-lead ECG. Incidence of this syndrome in a Japanese hospital-based study has been described in 1–2 % of patients with ischaemic stroke acutely [32]. A similar incidence has been reported in patients with subarachnoid haemorrhage [33]. Tokotsubu syndrome has a predisposition to females, with stroke affecting the insular cortex and brain stem involvement [34].

Both chronic heart failure and ischaemic stroke represent manifestations of similar underlying risk factors, such as diabetes and hypertension [35]. However, present studies regarding additional risk factors for stroke in patients with heart failure are inconsistent. For example, whilst retrospective analysis of the prospective Survival and Ventricular Enlargement (SAVE) study reported no significant impact of hypertension (and diabetes) in 2,231 chronic heart failure patients [36], the prospective Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) study did [35]. The latter study revealed a hazard ratio of 1.9 (95 % CI, 1.1–3.1) for stroke when hypertension was present at randomization of 2,144 heart failure patients without concomitant atrial fibrillation. A history of hypertension has also been reported to be associated with an increased risk of hospitalisation for stroke (hazard ratio = 1.4; 95 % CI, 1.01–1.8) [37]. Hypotension and its association with increased stroke risk has been described in the REasons for Geographic And Racial Differences in Stroke (REGARDS) study [38]. The validity of the results have been questioned, however, in view of the fact that patients self-reported heart failure, stroke, and transient ischaemic attack diagnoses.

A review published in 2011 summarised the emerging data regarding chronic heart failure as a risk factor for ischemic stroke. In summarising the available literature, it notes that prior stroke, arterial hypertension, and diabetes are additional risk factors in male chronic heart failure patients. However, in women, stroke risk is reported to increase with concomitant atrial fibrillation, diabetes, and the degree of left ventricular (LV) dysfunction. Moreover, it comments that advancing age does not appear to be an additional stroke risk factor in chronic heart failure patients, despite the known rise in the prevalence of heart failure with advancing age [27].

There is currently no evidence base for antithrombotic therapy in stroke prevention for chronic heart failure patients in sinus rhythm; however anticoagulation is clearly indicated in chronic heart failure patients with concomitant atrial fibrillation [17, 39, 40]. Evident within the literature is the fact that chronic heart failure with or without atrial fibrillation is a common cause of ischaemic stroke. Close attention needs to be paid not only to modifying the vascular risk factors common to both stroke and chronic heart failure, such as diabetes and hypertension, but also to ensure optimal management of heart failure per se, when its diagnosis is first made. This may serve to be advantageous not only in reducing the mortality associated with a heart failure diagnosis in itself, but also (knowing its association with increased stroke risk) give rise to an advantageous side effect of potentially reducing the burden of stroke-associated neurological and neuropsychological sequelae that a patient with heart failure is predisposed to, in light of the aforementioned increased stroke risk a heart failure diagnosis brings.

Cardiac dysfunction after a stroke is manifested by a wide variety of arrhythmias, ECG changes, elevated cardiac markers, and haemodynamic instability, which can lead to cardiogenic shock and subsequent death, as we have already alluded to earlier in the chapter [1]. Arrhythmias post-stroke are reported in up to 51 % of patients after ischaemic stroke and 78 % of patients after haemorrhagic stroke and are thus a common occurrence [41].

There are a wide variety of arrhythmias that can occur after stroke, including sinus bradycardia, supraventricular tachycardias, atrial flutter, atrial fibrillation, multifocal ventricular tachycardia, torsades de pointes, and ventricular fibrillation [1, 41]. However, no accurate data is available from population studies measuring their exact frequency. Atrial fibrillation is the most common arrhythmia, accounting for approximately 10–20 % of ischaemic strokes, and is associated with worse outcomes and subsequent risk of future cerebral and systemic thromboembolism. Atrial fibrillation independently increases the risk of stroke fivefold [42] and doubles the risk of recurrent stroke [43]. Recurrent stroke risk is reportedly similar for both sustained and paroxysmal atrial fibrillation [44], both of which are optimally treated with anticoagulation. Timely detection of paroxysmal atrial fibrillation after ischaemic stroke is crucial when aiming to optimise the uptake of treatment with anticoagulants [45].

The Virtual International Stroke Trials Archive (VISTA) register is an international collaborative repository for stroke clinical trial data which has been collated and anonymised for use in exploratory analyses [46, 47]. Data from the VISTA register including 2,865 patients with ischaemic stroke suggested that serious cardiac events (including sudden death, symptomatic heart failure, coronary artery disease, ventricular tachycardia, and fibrillation) occurred more frequently in patients with atrial fibrillation than without atrial fibrillation (14.2 % vs 6 %, OR: 2.58, 95 % CI: 1.97–3.37) [48]. It was hypothesised in this study that increased early cardiac complications contributed to the adverse effects of atrial fibrillation on early mortality within 3 months (OR: 1.44, 95 % CI: 1.14–1.81) after adjusting for baseline characteristics [48]. Of importance from another analysis from the same registry, the rate of first serious cardiac events peaked between day 2 and day 3, and a number of predictive variables were associated with the occurrence of serious cardiac adverse events [2]. These included a past history of heart failure, diabetes mellitus, elevated creatinine, increasing stroke severity, and prolonged QTc interval or ventricular extrasystoles on ECG [2]. Prolonged QTc interval changes on ECGs have been related to insular cortex involvement with subsequent alteration in autonomic tone, leading to increased sympathetic tone [49]. In fact, it has been shown that in patients with right insular involvement, increased QTc interval and left bundle branch block on ECG independently predict vascular mortality [50]. Moreover, right insular involvement may lead to increased risk of tachyarrhythmias and cardiac death post-stroke [51].