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228 Congestive Heart Failure in Diabetic...!
How it is Different?

left ventricular filling pressures, less exercise toler- and macrophage infiltration than tissue from patients
ance and more need for hospitalization without DM. and impaired platelet aggregation and
adhesion wtih consequent higher risk of thrombo-
PATHOPHYSIOLOGY sis. Angiographic examination of patients with DM
and unstable angina has shown a higher incidence
The pathophysiological basis of the relationship be-
tween CHF and DM may involve several possible of plaque ulceration and intracoronary thrombus for-
scenarios, that further potentiate each other (figure 1) mation than subjects without DM.
Results from the Framingham heart study demon-
DM may increase the risk of CHF through in-
creased risk for CAD and subsequent progression strated that patients with DM are at increased risk of
to post-ischemic CHF. In addition, DM may induce developing CHF following myocardial infarction with
myocardial alterations directly altering cardiac struc- worse outcome compared to non-diabetic patients
ture and function. (diabetic cardiomyopathy) Finally
(13)
CHF may induce insulin resistance and the subse- CONGESTIVE HEART FAILURE INDUCED
quent progression to DM. Type 2 Diabetes
Congestive heart failure (CHF) is an insulin-resistant
Post-ischemic Congestive Heart Failure in sate which constitutes the main risk factor for the
Diabetes: development of non-insulin dependent diabetes mel-
litus (NIDDM)
Patient with DM show a 2-4 fold increase in the rela-
tive risk of cardiovascular (CV) morbidity and mortali- CHF was associated with NIDDM independent of age,
ty compared to non-diabetic subjects.(14) In a Finnish sex age, family history of diabetes, body mass index,
population-based study, the risk of acute myocardial (BMI) waist / hip ratio,, and diastolic blood pressure.
infarction was 7-fold greater in patient with DM com- When untreated CHF patients where grouped into
pared to patients without a DM. suggesting that DM those with low (I and II) and high (III & IV)
is a CV risk equivalent
New York Heart Association (NYHA) classes, the as-
The pathophysiological basis for these adverse out- sociation of CHF and NIDDM was stronger with the
comes involves the hyperglycaemic milieu that exac- worsening of CHF .The mechanisms underlying this
erbates concomitant CV risk factors such as hyper- association are not fully understood, Sympathetic
tension dyslpidemia and activation of neurohormonal nervous system overactivity and consequent lipoly-
and inflammatory mechanisms resulting in accelerat- sis, activation of the renin–angiotensin-aldosterone
ed and more extensive CAD system (RAAS) and increased cytokine production
in CHF might play a roll in the development of insu-
Epidemiological studies show that subjects with insu-
lin resistance have an increased risk of incident CAD lin–resistance and consequent progression to type 2
even in the absence of overt DM . DM. CHF. may induced insulin resistance and in turn
triggers CHF in a vicious cycle..
Insulin resistance and consequent compensatory hy-
perinsulinemia is an early and central defect in the CONGESTIVE HEART FAILURE INDUCED
natural history of type 2 DM that may precede its BY CARDIOMYOPATHY
diagnosis by 10-20years. This defect is insulin ac-
tion, is associated with a cluster of abnormalities Patients with DM may develop a unique form of
referred to as the insulin resistance syndrome (or cardiac alterations termed diabetic cardiomyopathy,
metabolic syndrome) that contributes to endothe- defined as a defect in ventricular contractile function
lial dysfunction and progression toward advanced that is independent of CAD and hypertension. The
atherosclerosis. Diabetes mellitus is arteriopathic term diabetic cardiomyopathy describes myocardial
through a number of mechanisms. There include changes induce by diabetes – associated defects: in-
reduced vascular nitric oxide reduced prostacycline sulin-resistance and hyperglycemia which are central
production and enhanced endothelin, angiotensin II, drivers in several adaptive and maladaptive respons-
tissue factor activity and platelet activity. es ultimately inducing specific detrimental myocyte
abnormalities. several synergistic pathological mech-
When overt DM occurs hyperglycemia induced oxi- anism have been investigated as determinants of di-
dative stress may lead to a prothrombolic and proin- abetic cardiomyopathy .
flammatory state favouring the propensity to plaque
complications. Coronary tissue from patients with
DM exhibits a larger content of lipid-rich atheroma

GCDC 2017