|
Diabetes mellitus leads to many chronic complications. Vascular complications in the form of macroangiopathy accounts for lot of morbidity and mortality in diabetics.
Epidemiological datal
Incidence of coronary artery disease (CAD) is two fold more common in diabetic males and it is three fold more in female diabetics when compared to non diabetic population. With impaired G'TT the risk of CAD is increased three fold. 35% IDDM die of CAD between ages of 35-55. Those diabetics showing microalbuminuria having incipient nephropathy carry eight fold risk of CAD. 50% of diabetics show ischemic changes in ECG while they may be asymptomatic. When a diabetic patient gets admitted in ICCU with myocardial infarction, those who are poorly controlled as evidenced by elevated glycosylated haemoglobin, often get complications like cardiogenic shock and die. Painless infarct has been described in Framingham study in about 23%.
Etiopathogenesis of diabetic heart disease
Diabetic patient has accelerated atherosclerosis due to poor control and hyperinsulinaemia. This is further aggravated in the presence of hypertension. Even in the absence of CAD that is with normal coronaries primary cardiomyopathy can occur in diabetes mellitus and may present as biventricular failure. Their heart musculature show microvascular (small vessel) changes in the form of thickening and occlusion. Energy utilization in uncontrolled diabetes mellitus is characterised by non-utilization of carbohydrates and utilization of fatty acids and ketones.
Hypertension in diabetes mellitus
Patient may have systolic hypertension, hypertension related tc diabetic nephropathy and supine hypertension with orthostatic hypotension.2 The last named variety is difficult to treat and is often associated with diabetic peripheral neuropathy and autonomic neuropathy. Essential hypertension seen in diabetics may be related to increased sodium renal tubular absorption and increase in osmalarity in the uncontrolled state. Hyperinsulinaemia occurs in N1DDM due to peripheral insulin resistance; this state may be associated with excess sodium conservation in the body and this may predispose to hypertension. When there is syndrome X, there is obesity, hyper-insulinaemia, hyperlipidemia and hypertension.
Pathophysiology includes decreased sodium excretion by kidney, increase sympathetic activity independent of hypoglycemia, increased sensitivity to vasoactive stimuli and increase in vessel wall hypertrophy leading to peripheral vascular resistance. Excess insulin is atherogenic. In NIDDM there is low renin level. While planning treatment of hypertension in diabetics following points are to be kept in mind:
a) Therapy should not worsen the glycemic control
b) It does not alter the lipid profile
c) It does not worsen or unmask peripheral vascular disease. The first choice of drug
therapy is captopril/enalapril group of drugs.
Diabetes being a risk factor for CAD needs non invasive cardiac work up. Such workup can show 50% ischemic heart disease in a diabetic population. Holter, monitoring, exercise treadmill test and thalium myocardial scintigraphy after exercise or after dipyridamole in asymptomatic diabetics are of great value in diagnosing early CAD.
Myocardial infarction in diabetes mellitus:
Mortality in diabetics due to myocardial infarction in first week and first month is almost 2 fold when compared to non diabetic myocardial infarction. Increased mortality in this group is related to arrhythmia, CCF, LVF, and myocardial rupture. Mechanism involved may be LV dysfunction due to previous silent microinfarct and cardiac autonomic dysfunction. It is said that oral hypoglycemic agent-treated diabetic is more prone to get fatal arrhythmia like ventricular tachycardia and ventricular fibrillation during MI. Other arrhythmias which are noted are LBBB, sinus node dysfunction and AV conduction disorders.
ACE inhibitor drugs intervention in M.I.
Early administration of ACE inhibitors limit infarct size, prevent reperfusion injury and prevent left ventricular dilatation. They are indicated with larger Q in ECG, LVEF 40-45% and with CCF. The drug has to be started after 48 hrs. of MI when BP is stabilised and hypotension is not there.
Role of bradykinin in left ventricular regression
ACE inhibitors not only suppress angiotension II but also blocks degradation of bradykinin. This bradykinin has several favourable effects like arterial vasodilatation, inhibition of smooth muscle endothelial proliferation, stimulation of prostocyclin and nitric oxide.
ECG changes in diabetes mellitus (120 cases)3
| ECG |
No. of Cases |
Percentage |
| LVH |
6 |
5% |
| RVH |
10 |
8.25% |
| 1HD |
18 |
15% |
| Inferior MI |
1 |
8% |
| Anteroseptal Ml |
3 |
2.5%2.5% |
| Arrhythmia |
3 |
|
| Non-specific |
|
|
| ST Changes |
1 |
8% |
Prevalence of Ischemic ECG abnormalities in different categories : (shelgikar)4
| |
Men |
Women |
| Non D.M. |
5/66 (8%) |
6/50 (12%) |
| IGT |
9/43 (21%) |
5/29 (17%) |
| Diabetic |
14/119 (12%) |
15/66 (23%) |
(p 0.05 compared to non diabetics)
Diabetic cardiomyopathy
This occurs in diabetics independent of valvular, hypertensive and ischaemic heart disease. Histopathologically there are deposition of glycoprotein and abnormal collagen in the interstitial myocardial tissue, leading to increased stiffness of myocardium leading to diastolic dysfunction. Inframyocardial microcirculation is altered.
Clinically these patients are young diabetics with normal coronary angiogram. This state is characterised by prolonged L.V. relaxation, high left ventricular and diastolic pressure, increased myocardial stiffness index or impaired myocardial compliance.
Diabetic cardiac autonomic neuropathy5
Presence of cardiac autonomic neuropathy carries poor prognosis, such patients may have sudden death.
Resting tachycardia or a fixed heart rate are considered as characteristic features of cardiac denervation in diabetic cardiac autonomic neuropathy. The heart rate may not respond to reflex cardiovascular stimuli. There is reduced beat to beat variation, loss of nocturnal slowing of heart rate and abnormally fixed rates during cardiovascular stress. The denervated heart resembles transplanted heart.
Orthostatic hypotension is secondary to sympathetic post ganglionic denervation.
Echo findings in diabetes mellitus: (Goswami et al) Echo findings no. of cases 40
cases % age
|
M-Mode
|
a) Thickened
Ventricular Septum |
25 |
82% |
b) Thickened left
ventricular posterior
wall |
18 |
45% |
c) IVS
Ratio
LVP
more than 1.5 |
12 |
30%
70% |
d) a) Normal
Ventricular cavity
b) Large Ventricular '
cavity
c) Vigorous
contractors of left
ventricular posterior
wall |
17 |
41% |
Cardiovascular changes in diabetic ketoacidosis
Patients may have arrhythmias due to electrolyte disturbances, (U waves, ST-T
depression in ECG)
A. Hypokalemia (Serum K less than 3 mEQ/1) - Atrial arrhythmia, VPB
B. Hyperkalemia
a) Tall tented T waves at 5.5 - 7 mEQ
b) P wave amplitude reduced
c) PR prolonged with ST 7mEq depression
d) P disappears
e) Wide QRS
f) VF, VT - K > 10 mEq
Effect of acidosts :
With pH below 7.2 there is bradycardia and negative, inotropic effect, bicarbonate is given, in the presence of arrhythmia or hyperkalemia. In about 4% of cases in NIDDM, MI precipitates diabetic ketoacidosis. They carry poor prognosis because of LV pump failure.
During drug therapy of diabetic patients following precautions have to be taken. When nitrates are used in diabetics with autonomic neuropathy orthostatic hypotension is aggravated.
With the use of betablocker, insulin release from beta cell is affected and also it blunts the warning signs of hypoglycemia. Verapamil and nifedipine mildly impair glucose tolerance and the dose of antidiabetic drugs and insulin may have to increased. Sulphony lurea drugs are implicated in UGDP study to increase cardiovascular mortality.
While doing coronary angiography in diabetic nephropathy there is a danger that contrast media may precipitate acute renal failure.
In IDDM if coronary angiography is planned give half the morning dose of insulin prior to procedure and rest of the dose can be given after the procedure.
Conclusion
Causes of hypertension in diabetes and management are discussed. Risk of CAD increases in diabetes mellitus and its manifestations are outlined. For early diagnosis of IHD, stress test and Holter monitoring are very useful. In the presence of diabetic cardiomyopathy, arrhythmias and sudden death occur. Acute MI in uncontrolled diabetes carries greater risk of complication and mortality, while planning to treat CAD in diabetic, care should be taken in avoiding such drugs which may affect the glucose control.
REFERENCES
1. M.K. Chettri Cardiovascular disease in diabetes mellitus. In Practice of Diabetes
Mellitus in India by MMS Ahuja 1983 - Vikas Publishing House Pvt. Ltd. Chapter
12,pl06-117.
2. R.J.Dash and S. Singh. Hypertension and NIDDM in NIDDM supplement. JAPI
Editor. Siddharth Shah 1993, Chapter 14, p.66-69.
3. Abdul Hamid Zargar et al Electro- cardiographic evidences of autunomic dysfunction
in NIDDM, Jl. of Diabetic Association of India, 1993, Vol. 33 No.3, p.54.
Shelgikar KM, Sardesh BS, Naik SS, Yagnik CS Ischemic electrocardiographs
abnormalities in newly diagnosed Indian Type 2 diabetic subjects Novo Nordisk
diabetes update 1994 Proceedings p 127-129.
A.K. Das Diabetic autonomic neuropathy, Clinical features, diagnosis and
management, Novonordisk diabetes update 1994 p.29-32.
|
