Editorial
Heart-Brain Interactions:
Neurocardiology or
Cardioneurology Comes of Age
Clinical management of many disorders of the
heart and the brain cannot be viewed in isolation.
Cardiac issues often influence the care of neuro­
logic patients; likewise, neurologic considerations
are critical in several types of heart disease. The
neurologist cannot ignore the heart, and the car­
diologist must consider the cerebral consequences
of cardiac disease. A burgeoning clinical and
experimental literature supports the importance
of heart-brain and brain-heart relationships 1-6
(Table 1). These interactions are important and
common in everyday clinical practice.
Brain infarction and heart disease are linked
by several pathogenetic mechanisms. Coronary
artery disease, often asymptomatic, is common
in patients with transient ischemic attacks. 11,12
Most patients who experience transient ischemic
attacks will eventually die of a myocardial infarc­
tion.11 Asymptomatic stenosis of the carotid ar­
tery, even when severe, is a better predictor of
fatal myocardial infarction than is an ipsilateral
stroke. 13 " 15 Clearly, an aggressive surgical ap­
proach to both symptomatic and asymptomatic
atherosclerosis of the carotid artery must be tem­
pered by consideration of life-limiting coronary
artery disease.
Conversely, at least one in six ischemic strokes
is caused by cardiogenic embolism. 6 Many types
of heart disease can be sources of embolic frag­
ments, with atrial fibrillation and ischemic heart
disease predominating. Because many potential
cardioembolic sources are identifiable before em­
bolism, prevention would seem possible. In only
a fraction of patients with potentially embolo-
genic cardiac disease, however, does stroke ever
occur. Unless high-risk subgroups could be clin-
Address reprint requests to Dr. D. G. Sherman, University
of Texas Health Science Center at San Antonio, 7703 Floyd
Curl Drive, San Antonio, TX 78284.
Mayo Clin Proc 62:1158-1160, 1987
ically identified, many patients would need to be
treated to prevent embolism destined to occur in
only a minority. Currently available antithrom
botic therapy for potential prevention either is
associated with substantial risk or is of unproven
efficacy. Particularly when long-term anticoagu-
lation of elderly patients with relatively low risk
of embolism is considered, there is the fear that
the treatment may be worse than the disease.
Clinical studies to identify high-risk subgroups
of patients with potential cardioembolic sources
are needed.
Brain injury frequently complicates cardiac
surgical procedures, especially coronary artery
bypass grafting. 4,10 From 2 to 5% of patients who
undergo such a procedure experience periopera­
tive stroke attributable to a variety of mecha­
nisms, 4 and many others suffer more global
neuropsychoJogic impairment. 10 With more than
200,000 such bypass operations performed annu­
ally in the United States, techniques to minimize
brain injury are urgently needed. Irreversible
brain injury often determines the clinical out­
come of cardiopulmonary resuscitation. 7,8
In these clinical situations, as well as many
others, optimal care necessitates recognition of
heart-brain interactions. Cardiologists and neu­
rologists must continue to work together to refine
the concepts of these interactions and, in partic­
ular, their mechanisms and management. Neuro­
cardiology or cardioneurology has indeed come
of age.
In this issue of the Proceedings (pages 1077 to
1083), Dexter and colleagues further explore
heart-brain relationships in a population-based
study of the temporal relationship between isch­
emic heart disease and stroke. Surprisingly, the
risk of having a stroke after the initial diagnosis
of angina approximated that of a control popu­
lation (5.8% cumulative 10-year incidence). Even
inclusion of patients with stroke before the initial
diagnosis of angina would be unlikely to result
in clinically important differences. This observa­
tion suggests that early coronary atherosclerosis
is a poor marker of subsequent advanced cerebro-
vascular disease.
1158
Mayo Clin Proc, December 1987, Vol 62 EDITORIAL 1159

Of further interest, the increased risk of stroke Table 1.—Clinically Important Heart-Brain
after myocardial infarction was confined to the and Brain-Heart Relationships
time interval immediately after myocardial in­ Heart-brain Brain-heart
farction, and especially transmural myocardial Cardiac arrest and hypoxic- Transient ischemic attacks
ischemic encephalopathy 7,8 preceding cardiac death 11,12
infarction. This observation supports the hy­ Cardiogenic brain Ventricular arrhythmia after
pothesis that ventricular dyskinesia, maximal in embolism6,9 stroke 3
the peri-myocardial infarction period, leads to Cardiac surgical procedure Myocardial necrosis after
and neurologic injury10 stroke 3
stroke by means of embolization of intracardiac Cardiogenic syncope Carotid artery operation and
thrombi, 4 but it does not exclude hypotension, use Bacterial endocarditis perioperative coronary death
of anticoagulants causing brain hemorrhage, Reflex syncope
Role of central nervous system
and instrumentation as contributory causes of in hypertension
peri-myocardial infarction stroke.
In one reported study of 90 patients with stroke,
only 1 (1%) suffered acute myocardial infarction
during the first month after stroke, fewer than
other clinical reports. 16 Perhaps the exclusion of
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1160 EDITORIAL Mayo Clin Proc, December 1987, Vol 62

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