Clincal features of stable cad

2. Dr. Nisar Ahmad
CPEIC MULTAN
PAKISTAN

4.  Most patients with angina pectoris report of
retrosternal chest discomfort rather than frank
pain.
 The former is usually described as a pressure,
heaviness, squeezing, burning, or choking
sensation.
 Anginal pain may be localized primarily in the
epigastrium, back, neck, jaw, or shoulders.
Typical locations for radiation of pain are arms,
shoulders, and neck.

5.  Typically, angina is precipitated by exertion,
eating, exposure to cold, or emotional stress.
 It lasts for approximately 1-5 minutes and is
relieved by rest or nitroglycerin.
 Chest pain lasting only a few seconds is not
usually angina pectoris.
 The intensity of angina does not change with
respiration, cough, or change in position.
 Pain above the mandible and below the
epigastrium is rarely anginal in nature

6.  Ask patients about the frequency of angina,
severity of pain, and number of nitroglycerin
pills used during angina episodes.

9.  For most patients with stable angina, physical
examination findings are normal. Diagnosing
secondary causes of angina, and precipitating
factors is important.

10.  A positive Levine sign
(characterized by the
patient's fist clenched
over the sternum
when describing the
discomfort) is
suggestive of angina
pectoris.

11.  Look for physical signs of abnormal lipid
metabolism (eg, xanthelasma, xanthoma)
 diffuse atherosclerosis (eg, absence or
diminished peripheral pulses, increased light
reflexes or arteriovenous nicking upon
ophthalmic examination, carotid bruit).

12.  Examination of patients during the angina
attack may be more helpful.
 Useful physical findings include third and/or
fourth heart sounds due to LV systolic and/or
diastolic dysfunction
 mitral regurgitation secondary to papillary
muscle dysfunction

14.  Xanthomas are lesions characterized by
accumulations of lipid-laden macrophages.
Xanthomas can develop in the setting of altered
systemic lipid metabolism

21.  Patients with type III
present as adults with
premature
atherosclerosis and,
particularly, plane
(palmar) xanthomas

22.  Yellow infiltration of
palmer and digital
creases

24.  TG exceed
1000mg/dL
 Discreet yellow
papular lesions with
red base
 Buttocks back
,elbows,knees in
crops
 May coalesce and
form plaques

25.  Familial lipoprotein lipase
deficiency is an example of a
primary disorder in which a
deficiency of lipoprotein lipase
in tissue leads to a type I pattern
of hyperlipidemia, with a
massive accumulation of
chylomicrons in the plasma.
This effect results in a severe
elevation of plasma triglyceride
levels.
 Plasma cholesterol levels are
not usually elevated Eruptive
xanthomas are the most
characteristic skin manifestation
of this disorder.

26.  Plasma TG greater
than3000mg/dL

27.  Plasma TG 600mg/dL

29.  Small, yellow papules of
1-5 mm in diameter
 linear or reticular pattern
and may coalesce to form
plaques.
 The skin takes on a
plucked chicken, or
cobblestone appearance.
 Typically, first noted on
the lateral part of the neck
and later involve the
antecubital fossae; the
axillae; the popliteal
spaces; the inguinal and
periumbilical area

31.  The characteristic ocular
manifestations of
pseudoxanthoma
elasticum are angioid
streaks of the retina,
which are slate gray to
reddish brown
curvilinear bands that
radiate from the optic
disc. The streaks
represent cracks and
fissures in the calcified
Bruch’s membrane.

35.  Extensive tendon xanthomas but normal
plasma cholesterol levels
 Significantly elevated plasma levels of plant
sterols in the form of beta-sitosterol,
campesterol, and stigmasterol.
 Sitosterolemia is characterized by tendon and
tuberous xanthomas and by a strong
propensity toward premature coronary
atherosclerosis.

37. Can be found in
 pregnancy
 hypothyroidism,
 Cholestasis
 acute intermittent porphyria.

38. Can be associated with
 oral contraceptive use
 diabetes mellitus
 alcoholism
 pancreatitis
 gout
 sepsis due to gram-negative bacterial
organisms
 type I glycogen storage disease.

39. Can be found
 in nephrotic syndrome
 chronic renal failure
 Steroid thearpy
 immunosuppressive therapy

51.  Malar buterfly rash
red, confluent,
maculopapular rash
 Depigmentation and
scarring
 Livido reticularis
 Raynauds phenomena
 Symptomatic
coronary premature
atherosclerosis in 10%

53.  Lantern jaw,
coarsening of fascial
features,widly spaced
teeth,hypertrichosis,m
acroglossia, sphade
like hands
 Increased incidence of
premature CAD

56.  Saddle shaped nose
 Optic atrophy
 Argyll Robertson
pupil
 Coronary aorto-osteal
lesions due to aortitis

57.  Necrotizing arteritis of small and
medium sized vessels
 Palpable purpura
 Lividoreticularis It is a
dermatological disorder marked by
a mottled purplish discoloration of
the skin due to stagnation of blood
within the capillaries and venules.
It is a normal condition that occurs
more often during winter
“reticular”, referring to net-like
appearance
 Coronary arteritis in 50% of
patients

58.  Long smooth tapering lesions in healed state
 Fibrotic and hard

59.  In giant cell
arteritis/temporal
arteritis
 Bergers disease
 Takayasu disease
ostial lesions

62.  Hunter
 Hurler

63.  Malar flush
 Thin skin
 Lividoreticularis
 Downward lens
displacement
 Osteoporosis
 Mental retardation

64.  Fabry’s disease: Fabry’c (s):
 Febrile episodes
 Angiokeratomas/ alpha
galactosidase a deficiency
 Burning pain (peripheral
neuropathy of hands/feet)
 Renal failure
 youth death
 Ceramide trihexoside
(accumulated substrate),
 Cardiovascular disease

66.  Amylodosis

67.  Continous murmer
 Myocardial ischemia
 Angina coronary steal

68.  recently recognised
associations/causes of
coronary spasm
 Genral anesthesia
 Allergic angina
(histamin induced)
 Post partum
Bromocriptene use
 Neurofifromatosis
 Pheochromocytomas

69.  coronary artery
fibrosis after chest
radiation

71.  Emotional angina Angina with specific
psychological factors that
precipitate symptoms.
 Nocturnal angina Angina that awakens and
is sometimes associated with dreaming or
sleep apnea.
 Angina decubitus Angina that occurs shortly
after adopting the recumbent posture.

72.  Status anginosus Frequent, recurrent, sustained
angina refractory to usual treatment.
 Walk-through angina Angina with effort that
disappears gradually during activity that is sustained
(although usually at reduced intensity) and after which
improved exercise tolerance results.
 Second-wind angina A brief rest after an initial attack
results in a markedly improved threshold free from angina.
synonym is “warm-up” angina.

73.  Angina equivalents Symptoms other
than pain or discomfort that are ischemic
related and serve as angina surrogates, e.g.,
dyspnea, diaphoresis, fatigue, or light-
headedness.
 Silent angina Objective manifestations of
ischemia without symptoms.

74.  Crescendo angina Synonym is “accelerated”
angina. Change in the pattern of angina such
that it comes on more easily, lasts longer, or is
more frequent.
 Unstable angina A collection of symptoms
of angina usually incorporating crescendo
angina and/or acute coronary insufficiency.
By definition, unstable angina includes rest
pain.

75.  Postinfarction angina Symptoms that follow within
24 hours to 15days of acute myocardial infarction.
 Angina with normal CA Syndrome X or
microvascular angina.
 Variant angina Prinzmetal’s or vasospastic angina
related to epicardial coronary spasm. Pain often at
rest that is sustained and may have circadian
variation. Exercise tolerance often is normal.

76.  Right ventricular angina
 Anginal symptoms developing in
association with pulmonary hypertension
thought to be secondary to right ventricular
ischemia.