Hidoc Bulletin

Diabetics with advancing age accompanying symptoms like high blood pressure, excessive waist fat, and cholesterol imbalance induce poor metabolic control associated with microvascular and microvascular complications. CVD (Cardiovascular disease) threat develops with a mild increase in fasting blood glucose level before it touches to be diagnosed as diabetic. 

Diabetic risk factors enhancing CVD danger:
Obesity: Visceral fat-associated obesity provokes low-grade inflammation in diabetics and raises CVD danger. 

Epigenetics: A complex mechanism of connection between histone methylation and DNA causing obesity encourages diabetes-influenced CVD risk. 

Inflammation: Overexpression of cytokines caused by adipose tissue and activated macrophages establishes subclinical inflammation in obese diabetics with insulin resistance. Atherosclerosis and CVD develop when these cytokines join chronic inflammatory processes of vessel walls and induce lipid accumulation. 

Hyperglycemia: Acute hyperglycemia and glucose fluctuations decrease insulin sensitivity and increase T-cell loss, mitochondrial superoxide production, and endoplasmic reticulum stress by causing glucotoxicity, endothelium-dependent vasodilation, reduced myocardial perfusion, and inflammatory responses. 

Hypertension: High blood pressure can be observed before finding hyperglycemia. 

Hypertension: Along with diabetes initiates rapid oxidative stress-induced vascular dysfunction and injury. 

Dyslipidemia: Diabetics with dyslipidemia show a thermogenic profile consisting of enhanced very low-density lipoprotein cholesterol, triglycerides, and small & dense low-density lipoprotein cholesterol levels & reduced high-density lipoprotein cholesterol levels. 

Oxidative stress:Hexosamine and aldose reductase pathways get activated due to increased intracellular glucose concentrations. There is an oxidative load on mitochondria, increased production of reactive nitrogen species, and inflammatory cytokines. Also, there is a formation of advanced end products and the activation of protein kinase. Cumulatively these changes cause an increment in oxidative stress. 

Endothelial dysfunction: In diabetics, endothelium-dependent vasodilation disrupts reduced nitric oxide (NO) production from endothelial cells causing increased oxidative stress. Altogether in diabetics, imbalanced NO metabolism leads to microvascular complications. 

Cardiovascular autonomic neuropathy: Autonomic imbalance (ANS), inflammation, and CVD erupt in diabetics due to elevated inflammatory markers, increased sympathetic activity, and dysregulation of the autonomic nervous system. ANS destruction causes arterial stiffness, left ventricular hypertrophy, ventricular systolic dysfunction, and modulation of the sinus node, ventricular, and blood vessels. 

How to sharpen the joint care of diabetes and CVD? 

 ● Maintain good glycemic control by providing early hyperglycemia treatment 
 associated with metabolic memory protective effects
 ● Halt obesity by decreasing excessive visceral fat
 ● Manage dyslipidemia and aggressive atherosclerosis danger 
 ● Control hypertension co-occurrence and cardiovascular morbidity and mortality 
 ● Lower oxidative stress and slow down CVD progression
 ● Manage epigenetics influence increased body weight and fat level 
 ● Stop inflammatory cascade which promotes cardiovascular imbalance
 ● Disrupt endothelial dysfunction
 ● Avoid cardiovascular Autonomic Neuropathy (CAN) manifestation 
 ● Include mandatory screening schedule
 ● Follow a positive dedicated healthy heart care lifestyle 

Conclusion:

The key to reducing the burden of diabetes on the cardiovascular system is to identify the optimal time to introduce a suitable combination of personalized approaches & right disease-modifying agents. 

References

1. HEALTHCARE Eric Hong. indd,2018;52:49-52. www.eheartspecialist.com 
2. Cardiovasc Diabetol (2018) 17:83
3. Arterioscler Thromb Vasc Biol. 2019;39:558-568
4. DIABETES CARE, 2011;34 (2):S128-131 
5. Canadian Journal of Cardiology 34 (2018) 575e584