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140 Cardio Diabetes Medicine 2017

Heat Diabetes Hypertension
High Risk 1. Qualitative or quantitative lschemic
change in platelets
1. Atrial fibrillation 1. Large vessel atherothrombotic
2. Qualitative or quantitative disease
2. Left atrial or ventricular increase in procoagulant
thrombus and myxoma 2. Small vessel occlusive disease
activity
3. Dilated cardiomyopathy
3. Quantitative or qualitative 3. Hypertensive heart disease
4. Recent anterior wall MI decrease in antithrombotic Hemorrhagic
5. Mitral stenosis activity
1. Charcot-bouchard aneurysm
6. Endoca rditis Decreased fibrinolysis
7. Prosthetic valve 1. Decreased activity of t-PA 2. Acute hypertensive crisis
Low risk 3. Anurysmal sub-arachnoidl
2. Increased PAI-1 & alpha
haemorrhage
1. Congestive cardiac failure
2 antiplasmin
2. Dys/akinetic ventricular wall
3. Atrilal septal aneurysm
4. Mitral-valve prolapsed
5. Patent foramen ovale

Table 1 : Mechanism Of Stroke In Heart Disease, Diabetes And Hypertension

Caveats, controversies and captivating issues in the more randomized clinical trials are required to refute
management of these co-morbidities in the presence or recommend its use.
of stroke:
Conclusion
Management of hyperglycemia with insulin in the
acute phase of stroke is being followed for decades. Hypertension, diabetes and cardiac diseases play a
Recently interest has shifted towards use of oral an- major role in the pathogenesis and in deciding the
ti-diabetic drugs both for diabetic and non-diabetic final outcome of stroke. Stroke in turn affects these
indications. Metformin is shown to improve function- three entities adversely. Even though it appears as
al recovery after stroke if started weeks before stroke an oversimplification of the above discussed com-
or weeks after stroke in experimental animals. But, plex pathophysiological process, autonomic system
metformin in the acute phase is shown to be asso- dysregulation secondary to brain damage plays a key
ciated with increased infarct volume probably related role in the effects of stroke on heart, diabetes and
to neuronal AMPK activation leading on to increased hypertension.
lactate accumulation. Intravenous formulations of
glyburide is shown to reduce the risk of cerebral ede- References:
ma by acting on specific channel proteins involved in 1. Kopelnik A, Zaroff JG. Neurocardiogenic injury in neurovascular disorders.
the pathogenesis of cerebral edema. Critical care clinics. 2006 Oct 1;22(4):733-52.

In the management of hypertension during acute 2. Harada S, Fujita-Hamabe W, Tokuyama S. Ischemic stroke and glucose
phase of stroke the target blood pressure and the intolerance: a review of the evidence and exploration of novel therapeutic
targets. Journal of pharmacological sciences. 2012;118(1):1-3.
time to start therapy has to be individualised as it
is determined by multiple factors. In general vaso- 3. Johansson Å, Ahren B, Näsman B, Carlström K, Olsson T. Cortisol axis ab-
normalities early after stroke–relationships to cytokines and leptin. Journal
dilatory antihypertensive agents are to be avoided of internal medicine. 2000 Feb 1;247(2):179-87.
as they impair cerebrovascular auto regulation and 4. Dave JA, Engel ME, Freercks R, Peter J, May W, Badri M, Van Niekerk
there by worsen the ischemia. There are few studies L, Levitt NS. Abnormal glucose metabolism in non-diabetic patients pre-
to support the use of beta-blockers and/or ACE in- senting with an acute stroke: prospective study and systematic review.
hibitors for the management of hypertension in pa- QJM: An International Journal of Medicine. 2010 Apr 28;103(7):495-503.
tients with stroke as they are shown to decrease the 5. Qureshi AI. Acute hypertensive response in patients with stroke. Circula-
risk of infections especially pneumonia but further tion. 2008 Jul 8;118(2):176-87.

GCDC 2017