and M. Brandon Westover2
(1)
Harvard Medical School Department of Medicine, Brigham and Women’s Hospital, Boston, MA, USA
(2)
Harvard Medical School Department of Neurology, Massachusetts General Hospital, Boston, MA, USA
Abstract
Patients with stroke, coronary artery disease and peripheral vascular disease share some of the same risk factors and often live with one or more cardiovascular diseases. It is increasingly important for cardiologists to be familiar with the recognition and management of stroke (whether as a co-morbidity in a cardiac patient or as a complication from cardiac disorders or procedures).
Another important connection between neurology and cardiology is the cardiac manifestation of neurological disorders such as muscular dystrophies and Friedreich’s ataxia. They contribute significantly to the morbidity and mortality of such patients and often require cardiac consultation or procedures.
Abbreviations
ACA
Anterior cerebral artery
ACE
Angiotensin converting enzymes
ACS
Acute coronary syndrome
AF
Atrial fibrillation
ASA
Aspirin
AV
Atrioventricular
AVB
AV block
BP
Blood pressure
CMP
Cardiomyopathy
CTA
CT angiogram
DCM
Dilated cardiomyopathy
DVT
Deep venous thrombosis
ECG
Electrocardiogram
EMG
Electromyography
FA
Friedreich ataxia
HTN
Hypertension
ICA
Internal carotid artery
ICD
Implantable cardioverter defibrillator
ICH
Intracerebral hemorrhage
LBBB
Left bundle branch block
LV
Left ventricular
MAP
Arterial pressure
MCA
Middle cerebral artery
MD
Muscular dystrophy
PCA
Posterior cerebral artery
PFO
Patent foreman ovale
PVC
Premature ventricular complexes
RBBB
Right bundle branch block
RV
Right ventricle
RVH
RV hypertrophy
TIA
Transient Ischemic attacks
tPA
Recombinant tissue plasminogen activator
VF
Ventricular fibrillation
VT
Ventricular tachycardia
Introduction
Patients with stroke, coronary artery disease and peripheral vascular disease share some of the same risk factors and often live with more than one cardiovascular disease. It is increasingly important for cardiologists to be familiar with the recognition and management of stroke (whether as a co-morbidity in a cardiac patient or as a complication from cardiac disorders or procedures).
Another important connection between neurology and cardiology is the cardiac manifestation of neurological disorders such as muscular dystrophies and Friedreich’s ataxia. They contribute significantly to the morbidity and mortality of such patients and often require cardiac consultation or procedures.
Ischemic Stroke
Transient Ischemic Attacks (TIA)
Transient Ischemic attacks (TIA): reversible episode of focal neurologic symptoms; most last <1 h; must be <24 h by definition. Newer definition: brief, reversible episode of focal neurologic symptoms and negative MRI. Longer TIAs more likely to result from embolus, repeated similar TIAs suggest impending occlusion. Most TIAs should be worked up urgently, whether inpatient or outpatient. Early treatment and workup reduces risk of recurrent stroke by ∼80 % [1] (Tables 27-1 and 27-2).
Helps determine urgency TIA/stroke workup | Age ≥ 60 yo: 1 point | |||
Score ≥4 should have expedited workup | BP ≥140/90 mmHg: 1 point | |||
Stroke risk | Unilateral weakness (2 points) | |||
Score | Day 2 (%) | Day 7 (%) | Day 90 (%) | Speech impairment without weakness (1 point) |
<4 | 1 | 1.2 | 3.1 | |
4–5 | 4.1 | 5.9 | 9.8 | Duration: ≥ 60 min (2 points), 10–59 min (1 point) |
>5 | 8.1 | 11.7 | 17.8 | Diabetes: 1 point |
Table 27-2
CHADS2 score estimates of annual ischemic stroke risk in untreated atrial fibrillation
Factor | Points | Total points | Annual stroke risk (%) | |
|---|---|---|---|---|
C | CHF | 1 | 0 | 1.9 |
H | HTN | 1 | 1 | 2.8 |
A | Age ≥ 75 | 1 | 2 | 4.0 |
D | Diabetes | 1 | 3 | 5.9 |
S 2 | Stroke or TIA | 2 | 4 | 8.5 |
Total possible | 6 | 5 | 12.5 | |
6 | 18.2 |
Differential diagnosis for TIA/stroke: Top two mimics are seizures and migraine. Others: syncope, conversion, malingering, prior stroke re-manifested by toxic/metabolic derangement. The following “rules” of thumb are helpful, but not absolute, guides (Table 27-3).
Table 27-3
Differentiating TIA from seizures and migraines
Dx
Pts
Symptoms
Duration
TIA
Older, male, risk factors (HTN, DM)
Negative. If multiple modalities (e.g. sensory, motor) usually occur all at once
Brief (usually 15 min, can be longer)
Sometimes headache with symptoms
Seizures
Younger
Begins with positive symptoms. (e.g. tingling). Negative symptoms (e.g. paresis, aphasia) may follow
Very brief (sec – min). Postictal sx can last hours
Migraines
Younger, female, + FH
Headache after attack. Often associated with nausea, vomiting, photo/phonophobia. Begin with positive sx (e.g. seeing stars), then Negative sx. Sx evolve slowly (e.g. tingling slowly spreads up arm)
Longer (30 min up to hours)
Ischemic Stroke
Basic Mechanisms:
Embolic: Sudden symptom onset, usually maximal at onset.
Thrombotic: Main deficit sometimes preceded by warning signs (TIAs or minor symptoms) or stuttering/progressive course over several hours.
Common etiologies: Main subtypes of ischemic stroke (Table 27-4).
Table 27-4
Major subtypes of ischemic stroke
Large artery atherosclerosis (∼18 %)
Most common sites: carotid bifurcation, vertebrals at origin or at the vertebro-basilar junction, MCA at stem/bifurcation. Plaques rarely occur beyond first branching point. Risk factors: HTN, DM, dyslipidemia, smoking
Cardioembolic (∼21 %)
AF, MI, HF, prosthetic valves, rheumatic heart disease
Most often lodges in MCA (especially superior division) or PCA territory
Small embolus: cortical or penetrating arteries; large embolus: main branches
Small vessel (lacune) (24 %)
Due to severe atherosclerosis → thrombosis of small penetrating vessels
Infarcts up to 2 cm in size. Often associated with HTN
‘Unknown’ (∼34 %)
Paradoxical embolism. Falls under cryptogenic strokes: not lacunar, without evidence of cardioembolic (e.g. AF), or large artery source (e.g. carotid stenosis). Many are due to PFO
Uncommon stroke etiologies: (∼2 %)
Vasculitis: Due to autoimmune disease, arteritis (temporal, Takayasu), infectious (tuberculosis, syphilis, varicella zoster virus) or primary central nervous system vasculitis.
Dissections: Strokes in younger patients (age 35–50).
Fibromuscular dysplasia: Uncommon, affects women age 30–50. Imaging: segmental arterial narrowing and dilation (‘string of beads’). Arteries affected: renal, internal carotid artery (ICA) > vertebral > intracranial. Stenosis causes thrombosis or dissection.
Subcortical vascular dementia: Multiple subcortical infarctions cause dementia. Risk: chronic hypertension (HTN).
Drugs: Amphetamines, cocaine cause acute HTN or drug induced vasculopathy
Evaluation of ischemic stroke:
Urgent (in emergency department): CBC, BMP, PT, PTT, Cardiac Enzymes, non-contrast head CT to rule out intracerebral hemorrhage, (ICH) if considering treatment with IV tissue plasminogen activator (tPA).
Studies for secondary prevention:
Labs: Lipid panel, including lipoprotein(a), Hemoglobin A1c, homocysteine, TSH (looking for hyperthyroidism – increases risk of atrial fibrillation [AF]), ESR if suspecting vasculitis or endocarditis; Hypercoagulable panel for patients <50 years old (antiphospholipid antibodies, lupus anticoagulant, prothrombin G20210A gene mutation, factor V Leiden, protein C/protein S/antithrombin deficiencies) (Table 27-5).
Table 27-5
Hypercoagulable states that may lead to ischemic stroke
Association with ischemic stroke/cerebral venous thrombosis in younger pts <50 years. Strongest association with antiphospholipid antibody syndrome. Most guidelines recommend testing in pts <50 years old with venous thrombosis, no recommendations for acute ischemic stroke. Treatment: controversial, usually for venous thromboembolism: anticoagulation; for arterial thrombus (ischemic stroke) aspirin v. anticoagulation (except for Antiphospholipid antibody syndrome: anticoagulate)
Antiphospholipid Antibody Syndrome: Acquired, associated with autoimmune disease (e.g. lupus). Symptoms: recurrent pregnancy loss/thrombotic events. Diagnosis: Clinical event + 1 Lab abnormality: Antibodies against: cardiolipin and Beta 2 glycoprotein I lupus anticoagulant. If test abnormal, recheck in 12 weeks. Treatment: life-long anticoagulation
Prothrombin G20210A Gene Mutation: Causes ↑ liver synthesis of prothombin. Mostly in Caucasians
Factor V Leiden: Mutation in Factor V: becomes resistant to degradation (by activated protein C)
Protein C, Protein S, or Antithrombin deficiencies: Very uncommon. Diagnosis is difficult due to false positives, especially acutely after acute stroke. All three ↓ in acute thrombosis/surgery, or due hepatic dysfunction (i.e. decreased production), heparin decreases antithrombin, warfarin/OCPs decrease protein C/S
Brain Imaging: CT angiogram (CTA): for endovascular intervention/medical therapy (e.g. dissection, atherosclerosis, vasculitis), comparable to ultrasound for ICA stenosis; MRI/MR angiogram (MRA): very sensitive within first few hours; Carotid ultrasound if CTA or MRA not done.
24 h Holter for AF (longer if high suspicion).
Echocardiogram: rule out PFO or atrial septal aneurysm (in cryptogenic stroke), severe HF, thrombus, left atrial dilatation (increases risk for AF).
CT-Venogram of lower extremities: for + PFO and cryptogenic stoke, to rule out deep venous thrombosis (DVT)’s (Lower extremity ultrasound does not assess for DVT in iliac veins).< div class='tao-gold-member'>Only gold members can continue reading. Log In or Register to continue
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