Cardio-protection in acute stroke.
BACKGROUND
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
Literature review for influence of cardiovascular factors, specifically the value of NT proBNP (a sensitive index of cardiac impairment) for stroke mortality.


RESULTS
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.


CONCLUSIONS
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.
Sharma
Jagdish C
JC
Kings Mill Hospital, Sutton in Ashfield, Notts NG17 4JL, UK. jagdish.sharma@sfh-tr.nhs.uk
Ross
Ian
I
Vassallo
Michael
M
D000208:Acute Disease; D015415:Biomarkers / Q000097:blood; D002316:Cardiotonic Agents / Q000627:therapeutic use*; D015897:Comorbidity; D004359:Drug Therapy, Combination; D006331:Heart Diseases / Q000188:drug therapy* / Q000453:epidemiology / Q000503:physiopathology; D006801:Humans; D020097:Natriuretic Peptide, Brain / Q000097:blood; D018696:Neuroprotective Agents / Q000627:therapeutic use; D010446:Peptide Fragments / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology; D020521:Stroke / Q000188:drug therapy* / Q000401:mortality / Q000503:physiopathology; D015912:Thrombolytic Therapy
D015415:Biomarkers; D002316:Cardiotonic Agents; D018696:Neuroprotective Agents; D010446:Peptide Fragments; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain