Measures of damage limitation for
acute stroke have not produced substantial benefit to reduce
stroke mortality. Search continues for measures to reduce
stroke mortality.
METHODS: Cardiovascular factors, in particular
cardiac failure, adversely influence
acute stroke mortality. There is evidence of cardiological abnormality in
acute strokes as indicated by ECG changes and
tachycardia secondary to neurohumoral changes in
acute strokes. Patients with ECG abnormality,
tachycardia, dysrrhythmia and elevated levels of nor-
epinephrine in
acute stroke phase have higher mortality. Recent studies reveal that
Troponin (measure of cardiac injury) and
NT-proBNP (measure of cardiac function impairment) are elevated in
acute stroke patients, in response to the activated Renin-Angiotensin-Aldosterone-System and other neurohumoral changes, as a protective mechanism for sympatho-inhibitory activity. Patients with elevated
troponin have a higher mortality. Similarly elevated
NT-proBNP has been reported to be associated with higher short and long-term mortality. In one study all patients who died at 4 months had
NT-proBNP levels above the median, no patient with
NT-proBNP below the median value died. Two studies revealed that
NT-proBNP is more significant than clinical
stroke severity for
stroke mortality. Protection of myocardium in
stroke patients may be possible by the use of drugs such as beta-blockers and the drugs acting on RAAS. Reduction of mortality in studies of
candesartan (ACCESS study) and prior betablockers is one such example. Heart is at risk in
acute strokes and protecting heart makes sense to reduce
stroke mortality.
CONCLUSION: Some
stroke patients die due to occult cardiac damage and functional impairment in acute phase due to common risk factors. This relationship between brain and heart needs evaluation. Protection of heart with currently available or new drugs in
acute strokes is worth investigating since this intervention could be applied to a large proportion of
acute stroke patients over a wide time window.