Cardiovascular Laboratory Medicine Brenda Beckett, PA-C.

Cardiovascular Laboratory Medicine

Brenda Beckett, PA-C

Specimen Collection

Fasting– nothing to eat or drink for 10-12 hours– can have H2O and medication

Specific Tests to System

- Screening tests: Lipids, CRP, Homocysteine

- Identifying disease: BNP, cardiac enzymes

CV Screening Tests-Lipids

FASTING SPECIMEN Total Cholesterol HDL Triglycerides LDL - calculated or direct

Newest Guidelines

Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III), or ATP III

Screening

Can screen with Total Cholesterol, if >200, perform complete lipid profile

Screening should be performed on adults every 5 years

Normal Ranges are not determined as other lab tests - national standard

Total Cholesterol Levels

< 200 mg/dl

200-239 mg/dl

>= 240 mg/dl

Desirable, low risk for heart disease

Borderline high

High Cholesterol. In this range, a person has twice the risk of heart disease as person with <200 mg/dl

HDL-Cholesterol Levels

< 40 mg/dl

40-59 mg/dl

>=60 mg/dl

A major risk factor for heart disease

The higher the HDL, the better

Considered protective against heart disease

LDL-Cholesterol Levels

< 100 mg/dl

100-129 mg/dl

130-159 mg/dl

160-189 mg/dl

>=190 mg/dl

Optimal

Near Optimal/ Above Optimal

Borderline High

High

Very High

LDL-Cholesterol Levels

Target levels of LDL are adjusted if someone has existing risk factors for cardiovascular disease.

Tables, p 118 Wallach

Triglyceride Levels

< 150 mg/dl

150-199 mg/dl

200-499 mg/dl

>=500 mg/dl

Normal

Borderline High

High

Very high

Determining CV Risk

Identify presence of clinical atherosclerotic disease that confers high risk for coronary heart disease (CHD) events (CHD risk equivalent):

• Clinical CHD• Symptomatic carotid artery disease• Peripheral arterial disease• Abdominal aortic aneurysm

Note: Diabetes is regarded as a CHD risk equivalent.

Determining CV Risk, cont

Determine presence of major risk factors (other than LDL):

• Cigarette smoking• Hypertension (BP 140/90 mmHg or on antihypertensive

medication)• Low HDL cholesterol (<40 mg/dl)* HDL >60 counts as a

"negative" risk factor and removes one risk factor from count.• Family history of premature CHD (CHD in male first

degree relative <55 years; CHD in female first degree relative <65 years)

• Age (men 45 years; women 55 years)

Determining CV Risk, cont

Determine risk category:

• Establish LDL goal of therapy

• Determine need for therapeutic lifestyle changes (TLC)

• Determine level for drug consideration

Determining CV Risk, cont

LDL Cholesterol Goals for TLC and Drug Therapy in Risk Categories:

CHD risk equivalent <100 mg/dl

2+ risks <130 mg/dl

0-1 risk <160 mg/dl

Determining CV Risk, cont

Initiate therapeutic lifestyle changes (TLC) if LDL is above goal.

– Diet, weight management, physical activity.

Consider adding drug therapy if LDL continues to exceed goal.

http://www.nhlbi.nih.gov/guidelines/cholesterol/atglance.htm

Other Screening Tests

Homocysteine Amino acid in the blood. Increased homocysteine related to increased

risk of coronary heart disease, stroke and peripheral vascular disease.

Strongly influenced by diet - folic acid and vitamins B6 and B12 as well as by genetic factors

Other Screening Tests

CRP (Cardio or ultrasensitive) Traditionally used to diagnose and

monitor acute inflammatory states Mild CRP elevation (within the normal,

non-acute-phase range) has recently emerged as a valuable marker of cardiovascular risk.

Measured twice, 2 weeks apart.

Diagnosis of AMI

A number of laboratory tests are available.

None is completely sensitive and specific for MI, particularly in the hours following onset of symptoms.

Timing is important, as are correlation with patient symptoms, ECGs, and angiographic studies.

Diagnosis of AMI

CK, Total (Creatine Kinase): Simple, quick test. Not specific for MI. Three fractions: MM (skeletal muscle), MB (cardiac muscle), BB (brain tissue).

CKMB: Specific for cardiac injury. Rises 2-8 hrs after injury, returns to normal in 2-3 days. Serial testing every 4 hrs can provide a pattern.

Diagnosis of AMI

CKMB isoforms: – 1 and 2. Performed by electrophoresis. – Ratio of 2 to 1 can determine early cardiac

injury. – Labor intensive and not routinely used.

Diagnosis of AMI

Troponins I and T: Structural components of cardiac muscle. Released with injury. More specific than CKMB.

Rise within 3-12 hours, remain elevated for up to 2 weeks. Difficult to diagnose reinfarction, helpful with old MI.

Diagnosis of AMI

Myoglobin: Protein in skeletal and cardiac muscle. Sensitive but not specific. Rises early

LDH: Not used routinely. Need to measure isoenzymes.

On the horizon

h-FABP: Heart Fatty-Acid Binding Protein Early detection (as early as 20 min) Small cytosolic protein abundant in the heart Detects MI and reperfusion Renal clearance in few hours

Diagnosis of AMI - ACC guidelines

Typical rise and fall of biochemical markers (CKMB and Troponin) and at least one of the following:– Ischemic symptoms– New pathological Q waves on ECG– Ischemic ECG changes (ST elevation or

depression)– Coronary artery intervention

Case Study #1

30 yo male, admitted with CC of severe squeezing pain, lasted 10 min. Began after dinner. Radiated to L shoulder and jaw, assoc with palpitations, SOB. Similar episode 1 mo ago. Smokes 2ppd cigarettes.

FH: grandfather, father, sister all died from heart attacks at early age.

Case Study #1

PE: Pale, restless young man in severe distress due to 8/10 chest pain. Pain subsided after given nitro. BP 140/85, HR 90, RR 17, T 98F. Physical exam unremarkable.

ECG: Elevated ST segments in precordial leads.

Differential Diagnosis?

Case Study #1

What labs to order to confirm diagnosis?

Case Study #1

What further testing do you want to order?

Case Study #1

Diagnosis?:

CHF

BNP -B-type (brain) natriuretic peptide Useful for diagnosing CHF, predicting

morbidity and mortality, and maximizing therapy in these patients

First isolated from brain tissue, but is synthesized primarily in the ventricles of the heart.

NT-proBNP (isomer of BNP) testing has the same clinical utility as BNP

BNP

Increases glomerular filtration rate Decreases sodium retention, and

inhibits renin and aldosterone secretion. Marker of cardiac dysfunction that

correlates with the severity of symptomatic and asymptomatic left ventricular hypertrophy and CHF

CHF

Other laboratory findings in CHF: Anemia Renal function tests: may have prerenal

azotemia Lytes: hypokalemia, hyperkalemia,

hyponatremia

Bacterial Endocarditis

Blood culture: Proper collection, multiple collections

Pathogens: Strep viridans, S. aureus, Strep pneumoniae, enterococcus.

IV drug abusers: S. aureus

Hypertension

In primary hypertension, lab results can be normal.

Abnormalities may include: UA: hematuria, proteinuria, casts Lytes: potassium abnormalities FBS: screen for diabetes, metabolic

syndrome. Lipids: screen for atherosclerosis risk

Other Lab tests

PT - Prothrombin Time Includes INR - International Normalized

Ratio Used to monitor Coumadin therapy PTT - Partial Thromboplastin Time Used to monitor Heparin therapy (not

used with LMWH)

Case Study #2

47yo female admitted with cc of increasing SOB and fatigue. Past medical hx: cardiac arrhythmias, heavy alcohol consumption for many years and 40 pack year smoking history.

Case Study #2

PE: A&O, BP 100/65, HR 96, T 97.5F, RR 23.

Exam of neck showed distended jugular veins. Abdomen: protuberant abdomen with ascites. Liver and spleen not palpable. Pitting edema of LE.

Case Study #2

ECG: Sinus tachycardia and non-specific S-T segment changes.

CXR: No pulmonary infiltrates, no masses. Enlarged heart.

Labs?