Hypertension is the most common and important risk factor for stroke, and 60–70% of stroke patients have hypertension. However, elevated blood pressure is common in acute stroke patients even in those without underlying hypertension. During the first 1–2 days, an elevated blood pressure > 140/90 mmHg is observed in about 75% of patients with acute ischemic stroke and in more than 80% of patients with acute primary intracerebral hemorrhage. More than 50% of patients with acute stroke have systolic blood pressure > 160 mmHg. The elevated blood pressure is attributed to several factors, including neuroendocrine system-related stress response to acute stroke, stroke-related injury in autonomic center, increased intracranial pressure, or inadequately treated or untreated hypertension before the index stroke. The elevated blood pressure usually decreases spontaneously over the first week but sometimes over a few weeks in patients with severe stroke [6]. Therefore, the diagnosis of hypertension in patients with acute stroke can be made if patients have a history of use of antihypertensive agents or physician diagnosis before their strokes. For patients without a history of hypertension, the diagnosis can be made when the mean blood pressure in repeated measurements after the acute stage of stroke is ≥140/90 mm Hg.

Diagnosis of diabetes can be made if patients have a history of diabetes treatment of diagnosis before their strokes. For patients who do not have a clear history of prior diabetes, diabetes can be made by (1) an HbA1c value ≥6.5% on repeated tests, (2) a fasting plasma glucose level ≥ 126 mg/dL (7.0 mmol/L) on repeated tests, (3) a 2-h plasma glucose ≥200 mg/dL during a 75-g oral glucose tolerance test on repeated tests, or (4) typical hyperglycemic symptoms associated with a random plasma glucose ≥200 mg/dL.

About one-third of patients with acute stroke have prior or newly diagnosed diabetes. However, 44–68% of patients with acute stroke have hyperglycemia, and patients with severe stroke are more likely to have hyperglycemia. Underlying diabetes, the release of cortisol and norepinephrine in response to stroke-related stress, and relative insulin deficiency due to increased lipolysis in acute stroke contribute to hyperglycemia in acute stroke. Elevated glucose levels usually decline during the first week. Therefore, the diagnosis of new diabetes based on glucose level should be determined at least after 1 week from stroke onset. In contrast, HbA1c level reflects the 3-month average plasma glucose concentration and is less affected by acute stroke. Therefore, HbA1c level rather than glucose level would be better to newly diagnose diabetes and to assess pre-stroke glycemic status.

The previous National Cholesterol Education Program Adult Treatment Panel III set an LDL cholesterol target goal based on the patient’s risk category determined by the presence of atherosclerotic disease and major risk factors and then recommended how to achieve the target goal. In contrast, the updated 2013 American College of Cardiology and the American Heart Association guidelines do not specify a target LDL cholesterol goal. Instead, the guidelines recommend high-intensity statin (lowering LDL cholesterol by approximately ≥50%) or moderate-intensity statin (lowering LDL cholesterol by approximately 30–50%) in four major statin benefit groups who are at high risk of atherosclerotic cardiovascular disease events [7]. According to these guidelines, patients with ischemic stroke or TIA presumed to be of atherosclerotic origin are indicated for high-intensity statin therapy irrespective of their LDL cholesterol levels. For patients with ischemic stroke of non-atherosclerotic origin (cardioembolism, other determined etiology), statin therapy should be individualized based on their LDL cholesterol level, presence of diabetes, and 10-year estimated risk of atherosclerotic cardiovascular disease events. For patients with hemorrhagic stroke, there is debate on the risk and benefit of statin. Furthermore, in patients who were taking statins before their hemorrhagic strokes, the decision is more complex regarding whether to resume statins or not. After taking into consideration both the risks of future atherosclerotic cardiovascular disease events and recurrent hemorrhagic stroke, the decision should be individualized.

It is generally recommended to assess lipid profile during the acute stroke admission, and in-hospital LDL cholesterol levels can be used to guide decisions regarding long-term statin therapy. Since statin trials generally excluded patients with acute stroke, the benefit of statins in acute stage of ischemic stroke or TIA has not been confirmed. Observational studies and meta-analyses have suggested that statin therapy initiated during the acute ischemic stroke or TIA was associated with better functional outcome with a minimal risk. Furthermore, acute stroke hospitalization is a good opportunity to initiate statins and to increase the patients’ adherence.

Twenty to twenty-five percentage of patients with ischemic stroke or TIA have atrial fibrillation (AF), and long-term oral anticoagulation is strongly recommended otherwise contraindicated. AF is newly detected in about 10% of patients with acute ischemic stroke or TIA. Therefore, 12-lead electrocardiography (ECG) should be tested in all patients. However, covert paroxysmal AF is not easily detected by standard ECG. Patients who have stroke or TIA of presumed embolic origin should be additionally evaluated with 24-h ambulatory ECG monitoring, continuous ECG monitoring during stroke unit admission, or transesophageal echocardiography to detect occult AF.

However, despite cardiac evaluations and neuroimaging studies, 20–25% of patients have no clear embolic source, categorized as embolic stroke of undetermined source (ESUS). For these patients, outpatient prolonged ECG monitoring (generally up to 30 days) can be considered. The 30-Day Cardiac Event Monitor Belt for Recording Atrial Fibrillation After a Cerebral Ischemic Event (EMBRACE) trial demonstrated that, in patients with ESUS despite of standard tests including 24-h ECG monitoring, the noninvasive ambulatory ECG monitoring with a 30-day event trigger recorder compared to the standard 24-h ECG monitoring significantly improved the detection of AF. Within 90 days after randomization, AF was newly detected in 16.1% of the long-term monitoring group versus 3.2% in the 24-h ECG monitoring group [8]. In the Cryptogenic Stroke and Underlying AF (CRYSTAL AF) trial, the long-term ECG monitoring with an insertable cardiac monitor detected new AF in 8.9% of patients with ESUS, whereas the routine practice detected new AF in 1.4% of patients with ESUS within 6 months [9].

Stroke and coronary heart disease share common risk factors and pathophysiologic mechanisms. In addition, some cardiac conditions as well as AF are potential sources of cerebral embolism. More than one-third patients with ischemic stroke have overt or covert significant coronary artery stenosis. Therefore, during the acute stroke admission, transthoracic echocardiography can be considered as a routine examination to evaluate potential cardiac embolic sources and left ventricle wall motion. Patients with stroke or TIA are at high risk of coronary event as well as recurrent stroke, and the average 10-year risk of myocardial infarction is about 20% [2]. For patients who have a 10-year coronary heart disease risk >20%, or have significant stenosis in the major cerebral arteries, noninvasive testing for coronary artery disease may be considered [10].