Diagnostic cardiac.pptx fadhl salem fdrg

Cardiac Function ,
Lipid Profile Tests
Dr Mohammad Mansour

Cardiac enzymes
Clinical indications
Cardiac enzymes (markers of myocardial damage) should be measured in any
patient presenting with prolonged (<15min) ischaemic sounding chest pain. The
management of patients with acute coronary syndromes (ACS) (Figure), and the
diagnostic criteria for acute myocardial infarction have recently been redefined.
Indications for measurement of cardiac enzymes include
Patients presenting with ACS (unstable angina, non ST-segment elevation
myocardial infarction, Q-wave myocardial infarction).
Patients presenting with chest pain when the diagnosis of ACS is in doubt.
Routinely following percutaneous coronary intervention (PCI).
Routinely following surgical revascularisation (CABG).
Procedure
Venous blood is drawn from the patient on presentation and at 12#, 24, 48
and 72h after the onset of symptoms.

Possible results
Myocyte necrosis is detected biochemically when intracellular Macromolecules
leak from myocytes into the peripheral circulation. Myoglobin and the creatine
kinase MB isoenzyme (CK-MB), both non-specific markers, are released within
2h.
CK-MB2, a subform (isoform) of CK-MB 5MHZ has a higher sensitivity and
specificity.
The troponins (cTnT and cTnI) are part of the calcium-sensitive apparatus that
regulates the interaction of actin and myosin within cardiac myocytes;
troponins are specific for myocardial cell injury but may not be detectable for
6–12h (Figure).
Other ‘classic’ markers (AST, LDH) are unreliable and should not be used in the
diagnosis of myocardial damage.
The most sensitive early marker for myocardial infarction is CK-MB2 (91%)
followed by myoglobin (78%), thus a normal CK-MB2 subform at 6h reliably
excludes infarction. At 10h, the cTnI sensitivity is 96% with a specificity of 93%.

Interpretation
The diagnosis of ST-elevation myocardial infarction (STEMI) is usually obvious
from the appearance of the ECG, and is subsequently confirmed by elevated
cardiac enzymes.
Formerly, a subgroup of high-risk patients with ‘unstable angina’ was
recognized (also called minimal myocardial damage) with elevated levels of
cTnI and cTnT, but normal CK-MB.
These have now been reclassified as having sustained a non-ST-elevation
myocardial infarction (NSTEMI).
It is estimated that ~30% of patients presenting with ACS in the absence of
ST elevation would previously have been diagnosed as ‘unstable angina’, but
have in fact suffered myocyte necrosis (NSTEMI) using an elevation in cTnT
(>0.1μg/L) as the discriminator.

Pitfalls
Patients presenting very early following myocardial infarction may have
normal cardiac enzymes. Myoglobin and CK-MB may be detected as early as
2h, but cTnI and cTnT may not be significantly increased for 12h.
Troponins may also be released in acute myocarditis, pericarditis and in
patients with renal failure. Diagnosis of reinfarction (or extension) may be
impossible if relying on the troponins alone as they may remain elevated for
up to 14 days after the initial attack.

Estimation of Serum Triglycerides
Serum triglyceride analysis provides quantitative analysis of triglycerides, the
main storage form of lipids, which constitute about 95% of fatty tissue.
Although not in itself diagnostic, the triglyceride test permits early
identification of hyperlipidemia and the risk of CAD.
Elevated levels of triglycerides in plasma have been considered as risk
factors related to atherosclerotic diseases. The hyperlipidemias can be
inherited trait or they can be secondary to a variety of disorders of diseases
including nephrosis, diabetes mellitus, biliary obstruction and metabolic
disorders associated with endocrine disorders.
Reference Values
Females: 10 to 190 mg/dL (SI, 0.11– 2.21 mmol/L)
Males: 44 to 180 mg/dL (SI, 0.44–2.01 mmol/L)

Abnormal Findings
Elevated Levels in:
• Acute myocardial infarction • Alcoholism
• Anorexia nervosa • Hypothyroidism
• Chronic ischemic heart disease • Cirrhosis
Glycogen storage disease • Gout
• Hyperlipoproteinemia • Hypertension
• Impaired glucose tolerance • Nephrotic syndrome
• Pancreatitis (acute and chronic) • Obesity
• Pregnancy • Renal failure
• Respiratory distress syndrome • Stress
• Viral hepatitis • Werner’s syndrome
• Biliary obstruction • Diabetes mellitus
• Alcohol overconsumption • Endocrinopathies
• Congenital hyperlipoproteinemia • Nephrotic syndrome

Decreased in:
• Brain infarction
• Chronic obstructive lung disease (COPD)
• End-stage liver disease
• Hyperparathyroidism
• Hyperthyroidism
• Hypolipoproteinemia and a--lipoproteinemia
• Intestinal lymphangiectasia
• Malabsorption disorders
• Malnutrition

Purpose
• To screen for hyperlipidemia or pancreatitis
• To help identify nephrotic syndrome and poorly controlled diabetes
mellitus
• To assess coronary artery disease (CAD) risk
• To calculate the low-density lipoprotein cholesterol level using the
Friedewald equation

Investigation of hyperlipidaemia
Primary dyslipidaemias are relatively common and contribute to an individual’s risk
of developing atheroma (e.g. CHD, CVD). Prominent examples include familial
combined hyperlipidaemia (FCHL, ~2–3% of UK population) and heterozygous
familial hypercholesterolaemia (FH, UK incidence 1 in 500).
Major hypertriglyceridaemia also predisposes to pancreatitis.
The key features of familial FH, FCHL and diabetic dyslipidaemia are considered later.
Investigations
Although many subtle alterations in plasma lipids have been described, therapeutic
decisions rest on measurement of some or all of the following in serum or plasma
(plasma being preferred since it can be cooled rapidly):
Total cholesterol (may be measured in non-fasting state in first instance since
levels are not greatly influenced by meals).
Triglycerides (after 12h fast).
Low-density lipoprotein (LDL)-cholesterol (calculated using the Friedewald formula
when triglycerides are <4.5mmol/L):

 HDL-cholesterol (regarded as the ‘cardioprotective’ subfraction— HDL
particles are synthesised in the gut and liver and thought to be involved in
‘reverse transport’ of cholesterol from peripheral tissues to the liver where it
can be excreted as bile salts.
Notes on sampling in relation to lipoprotein metabolism
 Triglycerides (triacylglycerols) are measured after a ~12h overnight fast in
order to clear diet-derived chylomicrons.
 Alcohol should be avoided the evening prior to measurement of
triglycerides (can exacerbate hypertriglyceridaemia).
 A weight-maintaining diet is recommended for 2–3 weeks before testing.

 Lipid measurements should be deferred for 2–3 weeks after minor illness
and 2–3 months after major illness, surgery or trauma since cholesterol may
be temporarily and triglycerides . Following acute myocardial infarction it
is generally accepted that plasma cholesterol is reliable if measured within
24h of the onset of symptoms.
 The effects of certain drugs on lipids should be considered (see table).
 Glycaemic control should be optimised wherever possible before
measuring plasma lipids in patients with diabetes.

Important additional considerations are
 Day-to-day variability—generally, decisions to treat hyperlipidaemia
should be based on more than one measurement over a period of 1–2
weeks.
 Exclusion of secondary hyperlipidaemia—many common conditions,
drugs and dietary factors can influence plasma lipids (see table).
 Family members should also have their plasma lipids measured if a
familial hyperlipidaemia is suspected in a proband.
Both cholesterol and triglycerides may be affected to some degree by these
factors, but one often predominates. Pre-existing primary hyperlipidaemias
may be exacerbated.

Clinical features
E.g. xanthelasma, tendon xanthomas, etc. should always be sought.
A detailed family history, drug history and medical history (for diabetes and
other cardiovascular risk factors such as hypertension) should always be
obtained.
Certain endocrine disorders, impaired hepatic or renal function can
influence circulating lipid composition and cardiovascular risk.
A classification of the major familial dyslipidaemias is presented in the table
below.
 Specialist advice should be sought in the management of major or
resistant hyperlipidaemias.

Clinical Significance
The major plasma lipids of interest are total cholesterol and the triglycerides.
When an elevation of these plasma lipids is observed, the condition is called
hyperlipidemia. Cholesterol and triglycerides can be used to detect numerous
types of hyperlipidemia.For patients without clinical evidence of coronary or
other atherosclerotic vascular disease, the NCEP recommends health
screening, including measurement of TC and HDL cholesterol, at least
once every 5 years.
Further evaluation is performed for those patients with a high TC, low HDL
cholesterol (<35 mg/dL), or borderline TC who have at least two CAD risk
factors (age > 45 for men, > 55 for women or postmenopausal state without
estrogen replacement, high blood pressure, smoking, diabetes, HDL < 35
mg/dL, or a family history of CAD before age 55 in a male first-degree relative
or before age 65 in a female first-degree relative).
This evaluation should include fasting levels of TC, triglyceride, and HDL. LDL is
then calculated by applying the following formula:

(This formula is valid only when triglyceride is <400 mg/dL. A high HDL level
[>60 mg/dL] is considered a negative risk factor and reduces the number of
risk factors by one.)
The NCEP recommends that treatment decisions be based on the calculated
level of LDL. For patients with an elevated LDL (≥160 mg/dL) who have fewer
than two risk factors in addition to elevated LDL and who do not have clinical
evidence of atherosclerotic disease, the goal of treatment is an LDL level less
than 160 mg/dL. For those who have at least two other risk factors, the goal
of treatment is an LDL level less than 130 mg/dL. When LDL levels remain
higher than 160 mg/dL despite dietary measures, and the patient has two or
more risk factors (in addition to high LDL), or when LDL levels remain higher
than 190 mg/dL even without added risk factors, the addition of drug
treatment should be considered.

For those with CAD, peripheral vascular disease, or cerebrovascular disease,
the goal of treatment is an LDL less than 100 mg/dL.
All patients with clinical evidence of coronary or other atherosclerotic
disease should be evaluated with a fasting blood sample for measurement
of TC, triglyceride, and HDL. LDL is calculated.
In contrast to plasma TC, it is unclear whether plasma triglycerides are
independent risk variables.
A triglyceride level of less than 200 mg/dL is considered normal, 200 to 400
mg/dL is borderline high, and greater than 400 mg/dL is high.
Hypertriglyceridemia has been associated with diabetes, hyperuricemia,
and pancreatitis (when levels are > 600 mg/dL).

Cholesterol is a fat-like substance that is found in all body cells. The liver
makes all of the cholesterol the body needs to form cell membranes and to
make certain hormones.
The determination of serum cholesterol is one of the important tools in the
diagnosis an classification of lipemia. High blood cholesterol is one of the
major risk factors for heart disease.
Estimation of Serum Cholesterol (Total)

Serum cholesterol varies from 150-240 mg/100 ml in healthy young adults.
The level rises with age and may go upto 300 mg/100 ml in the elderly.
An increase in serum cholesterol (hypercholesterolaemia) is found in
diabetes mellitus, nephritic syndrome, obstructive jaundice,
hypothyroidism,
xanthomatosis and during ether anaesthesia. An idiopathic
hypercholesterolaemia of unknown actiology occurs in some families.
Hypercholesterolaemia, from any cause, predisposes to atherosclerosis.
A decrease in serum cholesterol (hypocholesterolaemia) is found in
hyperthyroidism, hepatocellular damage, anaemia (except haemorrhagic),
acute infections, wasting disease, intestinal obstruction and terminal states
of a variety of disease.

Low Density Lipoprotein (LDL) “Bad cholesterol”
High levels are linked to an increased risk of heart and blood vessel disease,
inlcuding coronary artery disease, heart attack and death. Reducing LDL
levels is a major treatment target for cholesterol-lowering medications.
Goal values:
Less than 70 mg/dL for those with heart or blood vessel disease and for
other patients at very high risk of heart disease (those with metabolic
syndrome)
Less than 100 mg/dL for high risk patients (e.g., some patients who have
multiple heart disease risk factors)
Less than 130 mg/dL for individuals who are at low risk for coronary artery
disease

Preparation:
Blood should be collected after a 12-hour fast (no food or drink, except
water). For the most accurate results, wait at least 2 months after a heart
attack, surgery, infection, injury or pregnancy to check LDL levels.
LDL is a lipoprotein (a combination of fat and protein) found in the blood.
It is called "bad" cholesterol because it picks up cholesterol from the blood
and takes it to the cells. A high LDL level is related to a higher risk of heart
and blood vessel disease.

Diagnostic cardiac.pptx fadhl salem fdrg

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