Cardiomyopathy plus diabetes and the heart Flashcards

1
Q

Definition of cardiomyopathy

A

Disease with the dominant feature being direct involvement of the myocardium.

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2
Q

Classification of cardiomyopathy

A

Functional

  • Dilated
  • Hypertrophic
  • Restricted

Specific aetiology

  • Ischaemic
  • Hypertensive
  • Inflammatory
  • Alcoholic
  • Post tachycardia
  • Drug induced (e.g. daunorubicin, adriamycin, peripartum etc)
  • Related to muscular or neuromuscular diseases
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3
Q

Dilated cardiomyopathy

A

Characterised by cardiac enlargement and reduced systolic function.

Although multiple diseases are known to cause it, most new cases are ‘idiopathic’.

All chambers (usually) enlarged with widespread fibrosis.

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4
Q

Presentation of DCM

A
  • Symptoms of LVF principally SOBOE.
  • Incidental finding of ECG changes often LBBB.
  • Incidental finding of big heart on CXR
  • Incidental big heart on echo or reduced LV function.
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5
Q

Management of DCM

A

Symptomatic: treat as LVF

  • ACEI (or ARBs) and vasodilating beta blockers the key drug classes.

Asymptomatic: treatment not certain. Generally use vasodilating beta blockers (e.g. carvedilol)

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6
Q

Hypertrophic cardiomyopathy

A

HOCM (however, not all obstructive).

Familial HOCM: autosomal dominant with variable penetrance and expression.

  • A number of genes are involved in development of HOCM including ones affecting myosin, others tropomyosin, others troponin T etc.
  • Many sporidic cases are presumably spontaneous mutation.
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7
Q

Pathophysiology of HOCM

A
  • Marked LVH often mainly septal
  • Small LV cavity
  • Often systolic anterior motion of MV

Septal LVH plus contribution from the MV movement may cause significant obstruction of LV outflow tract

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8
Q

Symptoms of HOCM

A
  • Generally asymptomatic and often found by family screening after index case.
  • Commonest symptom dyspnoea
  • Angina, palpitations, dizziness may occur.
  • Unfortunately sudden death may be first symptom or event
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9
Q

Examintion findings in HOCM

A
  • Forceful apex beat sometimes a double impulse (palpable ‘a’ wave).
  • Carotid pulse ‘jerky’
  • Often 4th heart sound
  • Mid-systolic murmur that changes with ‘vaso-active’ manouvres; increases with those that reduce venous return (smaller cavity magnifies LV outflow gradient) and decreases if LV volume increases.
  • Longer systolic mumur if MR also present.
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10
Q

Complications of HOCM

A
  • Sudden cardiac death (Commonest cause of SCD in adolescents)
  • Ventricular and SV dysrhythmias
  • CCD
  • Mitral regurgitation
  • Infective endocarditis
  • AF tolerated poorly
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11
Q

Management of HOCM

A
  • Echo confirms diagnosis
  • NO hihly competitive sports
  • If significantly symptomatic with LVOT gradient beta block and add if needed Ca channel blocker that reduces contractility such as verapamil
  • These drug classes reduce contractility and lessen the LVOT gradient
  • If gradient very large and patient very symptomatic surgical myomectomy (septal artery ablation sometimes used).
  • Defibrillator for patients at high risk of SCD
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12
Q

Restrictive cardiomyopathy

A

Also called infiltrative cardiomyopathy

Least common form of CM.

Management very difficult.

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13
Q

Restrictie CM aetiology

A

Amyloid, sarcoid and ‘idiopathic’ most common aetiologies.

Often hard to diagnose aetiology, sometimes requiring biopsy and even then not always helpful.

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14
Q

Restrictive CM pathophysiology

A

Principal pathophysiology is diastolic dysfunction and sometimes there is minimal systolic dysfunction.

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15
Q

Type I diabetes and CVD risk

A

Increased CVD risk appears related to increased weight gain particularly central adiposity (?) due to peripheral hyperinsulinaemia.

Risk is increased because of adverse effects of diabetic microangiopathy especially renal.

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16
Q

Type II diabetes and CVD risk

A

CVD rates are 4-10x higher than those od nondiabetics.

  • Metabolic syndrome with lipid abnormalities (high LDL, low HDL, high triglycerides) common.
  • HTN common
  • CVD remains high even with tight control of lipids and BP.
  • Same risk fo MI as someone with known CAD
17
Q

Why are type II diabetic at increased with of CVD?

A
  • Increased prothrombotic state
  • Stickier platelets
  • Increased endothelial dysfunction
  • Xs smooth muscle proliferation
18
Q

Features of diabetic CAD

A
  • Greater atheromatous plaque burden
  • Smaller vessel size
  • Disease more diffuse with longer narrowings
  • Generally mutiple arteries involved
19
Q

Management of diabetic CAD

A
  • Rigid control of lipids and BP
  • No evidence that rigid control of glycaemia improves outcome and some to the contrary
  • ACEI and ARBs for BP control
  • Standard treatment for angina with exception of revascularisation choices; CABG better than PCI
  • Higher restonosis rates with PCI
20
Q

Diabetic cardiomyopathy definition, characteristics and management.

A
  • Diabeted CM appears to be a distinct entity but is a diagnosis that is made after exclusion of significant CAD, H/T or valvular disease.
  • It is characterised by the presence of abnormal myocardial performance and/or structure in the absence of the above.
  • Management of the diabetic risk factors and usual treatment of a dilated cardiopathypathy.