Cardiac cephalgia

Introduction
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By Douglas J Lanska MD MS MSPH

Failure to recognize cardiac cephalgia can have serious consequences, including development of myocardial infarction or death. Furthermore, inappropriately treating cardiac cephalgia as migraine can result in severe morbidity or mortality, especially because vasoconstrictor medications used to treat migraine (eg, triptans and ergotamines) are contraindicated in acute myocardial ischemia.

In the International Classification of Headache Disorders diagnosis of cardiac cephalgia is based on the following criteria (Headache Classification Subcommittee of the International Headache Society 2004):

Cardiac cephalgia (ICHD 10.6)

  • Headache aggravated by exertion
  • Headache accompanied by nausea
  • Headache develops concomitantly with acute myocardial ischemia (during treadmill or nuclear cardiac stress testing)
  • Headache resolves and does not recur after effective medical therapy for myocardial ischemia or coronary revascularization

Synonyms

  • Anginal cephalgia
  • Anginal headache
  • Cardiac cephalgia
  • Cardiac migraine
  • Headache angina
  • Walk headache

Stem-and-leaf plot of age of 18 patients with cardiac cephalgia
(range 40 to 78 years, mean 61 years, median 60.5 years)

Ages
Cases
40s 017
50s 788999
60s 22777
70s 1158

Location of reported head pain (varies, without clear pattern)

  • Jaw
  • Teeth/gums
  • Tongue
  • Palate
  • Nose
  • Brow
  • Frontal or bifrontal
  • Unilateral retro-orbital
  • Bitemporal
  • Occipital
  • Mastoid
  • Ear
  • Vertex
  • Holocephalic

Accompaniments (vary, and may be absent)

  • Chest discomfort (typical, but isolated headache has been reported)
  • Nausea
  • Pain, numbness, or paresthesias in (usually left) shoulder and arm
  • Diaphoresis
  • Dyspnea

Precipitants

  • Exercise [typical, but can occur at rest (Gutiérrez-Morlote and Pascual 2002)]

Relieving factors

  • Rest (after several minutes)
  • Prompt relief with nitrates (most consistent characteristic establishing association with myocardial ischemia)
  • Resolution/prevention with antianginal medications
  • Resolution/prevention with coronary artery bypass grafting

Methods of confirming association between headaches and myocardial ischemia

  • Prompt relief with nitrates (whereas nitrates typically precipitate or worsen migraine, cluster, and tension-type headaches)
  • EKG during headache demonstrating ST-segment depression
  • Ambulatory EKG monitoring
  • Exercise stress testing
  • Thallium exercise stress testing
  • Reproduction of headache during angioplasty

Proposed mechanisms (none are entirely satisfactory, and more than 1 may be operative)

  • Concomitant vasospasm of coronary and cerebral vessels. This seems doubtful, because it would be unlikely for cerebral vasospasm to be so predictably time-linked with coronary vasospasm.
  • Referred pain. Lipton and colleagues and others point out that the heart's sympathetic fibers are supplied by cervical and thoracic ganglia that also supply structures of the eye, face, neck, and cerebral vessels (Bryhn and Hindfelt 1984; Fleetcroft and Maddocks 1985; Grace et al 1997; Lipton et al 1997; Green 2001). However, the basis for quite varied locations of head and facial pain in association with myocardial ischemic makes a strictly anatomic basis hard to conceptualize, and the numerous proposed pathways without adequate documentation also make this mechanism so far not totally convincing.
  • Increased intracranial pressure. Lipton and colleagues suggested that a sudden decrease in cardiac output associated with angina could produce increases in left ventricular and right atrial pressures, with resulting decreased venous return from the brain, and an increase in intracranial pressure (Lipton et al 1997). Such changes in intracranial pressure with angina have not been documented.
  • Release of a pain mediator with cardiac ischemia that acts on intracranial pain-sensitive structures.

    Note: In general, patients with exertional headache require neuroimaging, preferably with MRI, to exclude structural pathology (especially in the posterior fossa).

It is essential to distinguish cardiac cephalgia from migraine

  • Both may present with severe head pain, triggered by exertion, and accompanied by nausea
  • Vasoconstrictors are indicated for migraine, but contraindicated for cardiac cephalgia as they may constrict coronary arteries and thus precipitate a myocardial infarction.
  • Nitrates are indicated for cardiac cephalgia and may lead to prompt resolution of headache, whereas nitrates can induce headache in migraineurs.
  • Cardiac cephalgia should be considered in patients with exercise-related headache with onset after age 40, and particularly in those with vascular risk factors and de novo headaches after age 50.

Suggested clinical diagnostic criteria for cardiac cephalgia

Required:

  • Headache develops concomitantly with evidence of acute myocardial ischemia (eg, on EKG, treadmill stress test, or nuclear cardiac stress testing), typically (but not necessarily) precipitated by exertion
  • Acute headache relieved within several minutes of initiation of postexertional rest and/or administration of sublingual nitroglycerin and/or administration of other antianginal therapy (eg, oxygen, nitropaste, aspirin)

Supportive:

  • Age greater than 40 years
  • Headaches precipitated by exertion
  • Headaches do not recur after institution of antianginal medications or coronary revascularization
  • Presence of vascular risk factors
  • Known coronary artery disease