Diabetic cardiomyopathy presentation

1. Diabetic
Cardiomyopathy

2. • Diabetic cardiomyopathy has been defined as
ventricular systolic or diastolic dysfunction in a
patient with DM without other recognized cause
(such as CAD or hypertension).

3. There is limited evidence on the prevalence of diabetic
cardiomyopathy.
• A study of 2042 residents of Olmsted County aged ≥45
years found a community population prevalence among
individuals with DM, 16.9 percent met criteria for
diabetic cardiomyopathy.
• In a pooled cohort study that included patients with
diabetes, the prevalence of LV dysfunction varied from
7 to 12 percent. Among asymptomatic patients with
evidence of LV dysfunction, the five-year incidence of
symptomatic HF was 8 to 13 percent.
• There is some evidence that diabetic cardiomyopathy
is uncommon in patients with type 1 diabetes in the era
of intensive insulin therapy

4. Pathogenesis
A variety of derangements associated with DM may
contribute to ventricular dysfunction.
• Insulin resistance and hyperinsulinemia may cause LV
hypertrophy and associated diastolic dysfunction.
Diastolic dysfunction is highly prevalent in patients with
DM.
• Advanced glycation end product deposition may
increase LV diastolic stiffness and impaired cardiac
relaxation directly by cross-linking collagen, or
indirectly by enhancing collagen formation or reducing
nitric oxide bioavailability.

5. • Autonomic neuropathy may play a role in the
development of LV dysfunction . Sympathetic
stimulation increases LV contraction and also
increases LV relaxation rates, the latter perhaps by
facilitating calcium uptake by the sarcoplasmic
reticulum. Autopsy studies in diabetic patients have
found depleted myocardial catecholamine stores
which could impair both systolic and diastolic
function . These changes may be associated with
functional impairment in cardiac sympathetic nerve
fibers.

6. • The capacity of the vascular bed to meet metabolic
demands may be impaired by abnormal epicardial
vessel tone and microvascular dysfunction.
Diabetics have impaired endothelium-dependent
relaxation , a defect that may be related to
inactivation of nitric oxide by advanced glycation
end products and by increased generation of free
radicals . The abnormal vasodilator response in
diabetes extends to the coronary microcirculation.
Microcirculatory dysfunction in diabetics may be
due in part to downregulation of the expression of
vascular endothelial growth factor (VEGF).

7. • Decreased insulin availability or responsiveness can
impair energy-independent transport of glucose
across the cell membrane. Since ischemic
myocardium depends upon anaerobic metabolism
of glucose, increased glucose uptake and
metabolism are necessary for maintenance of
myocardial function . Diminished insulin activity
limits glucose availability, resulting in a shift toward
fatty acid metabolism. These changes increase
myocardial oxygen utilization and can reduce the
compensatory capacity of noninfarcted
myocardium.

8. • Other factors that may contribute include myocardial
accumulation of lipid and other toxic products of fatty
acid metabolism , impaired calcium handling ,
upregulation of the renin-angiotensin system ,
increased reactive oxygen species , and mitochondrial
defects.
• Pathologic changes in the myocardium have been
described in diabetic patients that may account for
observed functional changes . These include fibrosis,
infiltration of the interstitium with periodic acid-Schiff
(PAS)-positive material, and alterations in the
myocardial capillary basement membrane, including
the formation of microaneurysms.

10. Functional & Structural
Abnormalities
The following cardiac and hemodynamic alterations
have been observed in patients with Diabetes
mellitus:
• Higher LV mass, wall thickness, and arterial stiffness
and reduced systolic function compared with
individuals without DM. These abnormalities were
independent of BMI and blood pressure.

11. • Prolonged pre-ejection period and a shortened ejection
time, both of which correlate with reduced resting LV
ejection fraction (LVEF) and diminished systolic function
. Diabetic patients also have a lower LVEF in response
to exercise, suggesting a reduction in cardiac reserve.
• Diastolic dysfunction , which may be due in part to
increased LV mass. For example, an E/e' ratio >15 (a
marker of elevated LV diastolic pressure) was observed
in 23 percent of 1760 diabetic patients studied in
Olmsted County . Greater diastolic dysfunction has
been observed in diabetic patients with worse glycemic
control and in those who are also hypertensive. In an
observational study, HbA1c level correlated with E/e'
ratio.

12. • Pharmacologic therapy for HFrEF or HFpEF in adults
with DM is generally the same as for adults with
HFrEF or HFpEF given evidence of similar efficacy of
for nearly all agents in patients with or without DM.
• Glycaemic Control : ADA Recommend Peak Glucose
Levels less than 188 mg/dl and HBA1C less than 7.0
%.
• Healthy Diet
• Regular Exercise

13. Diabetes Mellitus
Gastrointestinal
Complications

14. • Long-standing type 1 and 2 DM may affect the
motility and function of the GI system.
• The most prominent GI symptoms are delayed
gastric emptying (gastroparesis) and altered small-
and large-bowel motility (constipation or diarrhea).
• Gastroparesis may present with symptoms of
anorexia, nausea, vomiting, early satiety, and
abdominal bloating.

15. • Although parasympathetic dysfunction secondary
to chronic hyperglycemia is important in the
development of gastroparesis, hyperglycemia itself
also impairs gastric emptying.
• Nocturnal diarrhea, alternating with constipation, is
a feature of DM-related GI autonomic neuropathy.

16. GI manifestations of DAN are diverse, and symptoms and
pathogenic mechanisms have been categorized according to
which section of the GI tract is affected:
• Esophageal enteropathy (disordered peristalsis, abnormal
lower esophageal sphincter function)
• Gastroparesis diabeticorum (nonobstructive impairment of
gastric propulsive activity; brady/tachygastria,pylorospasm)
• Diarrhea (impaired motility of the small bowel [bacterial
overgrowth syndrome], increased motility and secretory
activity [pseudocholeretic diarrhea])
• Constipation (dysfunction of intrinsic and extrinsic intestinal
neurons, decreased or absent gastrocolic reflex)
• Fecal incontinence (abnormal internal anal sphincter tone,
impaired rectal sensation, abnormal external sphincter)

17. The finding of retained food in the stomach after an 8- to 12-h fast in the
absence of obstruction is diagnostic of gastroparesis.
Gastroparesis interferes with nutrient delivery to the small bowel and
therefore disrupts the relationship between glucose absorption and
exogenous insulin administration. This can result in wide swings of glucose
levels and unexpected episodes of post-prandial hypoglycemia and
apparent “brittle diabetes.” Gastroduodenoscopy to exclude pyloric or
other mechanical obstruction
• Manometry to detect antral hypomotility and/or pylorospasm
• Double-isotope scintigraphy to measure solid-phase gastric emptying
Constipation.
• Constipation is the most common GI complication, affecting nearly 60%
of diabetic patients
• Anorectal manometry for evaluating sphincter tone
• Assessment of colonic segmental transit time.

18. • Current treatments for these complications of DM are inadequate
and nonspecific. Improved glycemic control should be a goal but
has not clearly shown benefit.
• Smaller, more frequent meals that are easier to digest (liquid) and
low in fat and fiber may minimize symptoms of gastroparesis.
Medications that slow gastric emptying (opioids, GLP-1 receptor
agonists) should be avoided. Metoclopramide may be used with
severe symptoms but is restricted to short term treatment.
• Symptoms of gastroesophageal reflux disease may require acid
blocking therapy with a histamine-2 receptor antagonist or
proton pump inhibitor.
• Diabetic diarrhea in the absence of bacterial overgrowth is
treated symptomatically.
• Gastric electrical stimulatory devices are available but not
approved.

19. General Measures To Prevent
Diabetes Related Complications:
• Glycaemic Control : ADA Recommend Peak Glucose
Levels less than 188 mg/dl and HBA1C less than 7.0
%.
• Healthy Diet
• Regular Exercise
• Maintaining Normal B.P
• Cessation of smoking
• Modest Alcohol intake
• Regular Follow-up