Dr Mohammad Ali Raza Qizalbash (Dr MARQ), Pakistan
[Diseases Risk factors/Prognosis/Mnemonics for USMLE STEP 3]
Sources used: MTB 2, MTB 3, MTB IM, FA 3, Step Up to Medicine, Step Up to Step 3
Cardiology
Coronary Artery Disease Risk Factors:
The most clearly agreed-upon risk factors for CAD are:
Diabetes mellitus
Tobacco smoking
Hypertension
Hyperlipidemia
Family history of premature coronary artery disease (Men 55 years; women 65 years)
Age above 45 in men and above 55 in women
The worst risk factor for CAD is diabetes mellitus, but the most common risk is hypertension.
{Common risk factors for atherosclerosis may be remembered by the mnemonic SHIFT MAID: Smoking,
HTN, Insulin resistance (NIDDM), Family history, Triglycerides and cholesterol (high), Male, Age
(increased), Inactivity, Diet}.
Less Reliable but Probable Risk Factors for CAD:
Physical inactivity
Excess alcohol ingestion
Insufficient fruits and vegetables in the diet
Emotional stress
Elevated cardiac CT scan calcium scores
Positron emission tomography (PET) scanning
Increased physical activity and exercise reliably lower all-cause mortality, but physical inactivity is
not as severe a risk for coronary disease as diabetes and hypertension
Calcium scores on a CT scan of the heart are still considered experimental. It is not clear what to do
differently with this information in addition to standard risk factors.
Unreliable (Unproven) Risk Factors for CAD:
Several disease markers such as elevated homocysteine levels, chlamydia infection, and elevated C
reactive protein levels have not proven to be reliable. There is no benefit to measuring, following, or
attempting to therapeutically intervene on these factors.
1
,CAD can have the following clinical presentations:
• Asymptomatic
• Stable angina pectoris
• USA pectoris
• MI—either NSTEMI or
STEMI
• Sudden cardiac death
Prognostic indicators of CAD:
a. Left ventricular function (ejection fraction [EF])
• Normal 50%
• If <50%, associated with increased mortality
b. Vessel(s) involved (severity/extent of ischemia)
• Left main coronary artery—poor prognosis because it covers approximately two-thirds of the heart
• Two- or three-vessel CAD—worse prognosis
{Stable angina prognosis
Is related to the ability to prevent progression of atherosclerosis and to control comorbid factors; left
ventricle function and the degree of left coronary artery occlusion are the strongest predictors of long-
term survival}.
{Unstable angina prognosis
Short-term prognosis is frequently predicted by the thrombolysis in myocardial infarction (TIMI) risk
score.
Long-term prognosis is best predicted by EF and the degree of residual ischemia detected on
posttherapy stress testing.
Up to 10% of patients will have a myocardial infarction or will die within 6 months following the onset of
new unstable angina.
One third of patients will have a myocardial infarction within 3 years after a new onset of unstable
angina}.
{MI Prognosis
there is a 30% acute mortality with 50% of survivors being rehospitalized within 1 year and 10% dying
within 1 year; complications include infarct extension, arrhythmias, myocardial dysfunction, papillary
muscle necrosis, wall rupture, aneurysm, mural thrombus, pericarditis, and Dressler syndrome (i.e.,
fever, pericarditis, and increased erythrocyte sedimentation rate [ESR] 2 to 4 weeks post-MI)}.
{The differential diagnosis for chest pain may be remembered by the mnemonic
CHEST PAIN: Cocaine/Costochondritis, Hyperventilation/ Herpes zoster, Esophagitis/
Esophageal spasm, Stenosis of aorta, Trauma, Pulmonary embolism/ Pneumonia/
Pericarditis/Pancreatitis, Angina/ Aortic dissection/ Aortic aneurysm, Infarction (myocardial),
Neuropsychiatric disease (depression)}.
{Treatment for MI may be remembered by the mnemonic Be MONA: Beta-blocker,
Morphine, O2, Nitroglycerin, ASA/ ACE-I}.
2
,CHF Risk factors:
CAD
HTN
valvular disease
cardiomyopathy
COPD
drug toxicity
alcohol use
{CHF due to systolic dysfunction
First medications given are typically loop diuretics (decrease heart preload) and either ACE-I or
angiotensin receptor blockers (ARB) (decrease preload and afterload and increase cardiac output).
β-blockers may be added once a stable ACE-I dose is prescribed and should not be administered during
acute exacerbations.
Digoxin (increases contractility) may be added to the regimen to improve symptoms but has not
demonstrated an ability to improve mortality.
Spironolactone or vasodilators may be added for persistent symptoms.
CHF due to diastolic dysfunction
BP is controlled with calcium channel blockers, ACE-I, or ARB.
β-blockers are useful to control the heart rate and to decrease cardiac workload in stabilized patients.
K-sparing diuretics should be given to reduce cardiac hypertrophy caused by aldosterone.
Recombinant BNP (i.e., nesiritide) has been shown to improve outcomes during severe acute
exacerbations.
Underlying conditions should be treated.
The patient should adhere to a low-salt diet.
Progressive cases may require cardiac transplant or implantation of an assistive device (indicated for an
ejection fraction below 35%)}.
{Frequent causes of CHF exacerbations are remembered by the mnemonic A SMITH
PEAR: Anemia, Salt, MI, Infection, Thyroid (high or low), HTN, Pericarditis, Endocarditis, Arrhythmia, Rx
(not taking medications)}.
CHF Prognosis:
Approximately half of patients with CHF will eventually die from a ventricular arrhythmia.
Hospital admission is associated with up to a 20% mortality rate.
Mortality increases to 40% in the presence of a comorbid MI and 80% in the presence of hypotension.
Hyperlipidemia Risk factors:
a. Diet
• Saturated fatty acids and cholesterol cause elevation in LDL and total cholesterol
• High-calorie diets do not increase LDL or cholesterol levels (are “neutral”)
but do increase triglyceride (TG) levels
• Alcohol increases TG levels and HDL levels but does not affect total cholesterol levels
b. Age—cholesterol levels increase with age until approximately age 65. The increase is greatest during
early adulthood—about 2 mg/dL per year
c. Inactive lifestyle, abdominal obesity
d. Family history of hyperlipidemia
3
, e. Gender—men generally have higher cholesterol levels than do women; when women reach
menopause, cholesterol levels then equalize and may even be higher in women than in men
f. Medications
• Thiazides—increase LDL, total cholesterol, TG (VLDL) levels
• β-Blockers (propranolol)—increase TGs (VLDL) and lower HDL levels
• Estrogens—TG levels may further increase in patients with hypertriglyceridemia
• Corticosteroids and HIV protease inhibitors can elevate serum lipids
g. Genetic mutations that predispose to the most severe hyperlipidemias
h. Secondary causes of dyslipidemia
Hypertension Risk factors:
Age—both systolic and diastolic BP increase with age.
Gender—more common in men (gap narrows over age 60); men have higher complication rates.
Race—it is twice as common in African-American patients than in Caucasian patients; African-American
patients also have higher complication rates (stroke, renal failure, heart disease).
Obesity, sedentary lifestyle, dyslipidemia.
Family history.
Increased sodium intake—this correlates with increased prevalence in large populations, although not in
individuals; individual susceptibility to the effects of high salt intake varies.
Alcohol—intake of more than 2 oz (8 oz of wine or 24 oz of beer) per day is associated with HTN.
Prognosis:
Untreated or poorly treated disease increases the risk of CAD, stroke, aortic aneurysm, aortic dissection,
CHF, kidney disease, and ophthalmologic disease.
Long-term prognosis is directly related to the ability to control BP, ability to reduce unhealthy behaviors,
and the avoidance of complications.
The behaviors that are risk factors for HTN are also associated with diabetes mellitus.
Hypertensive emergency:
Excessive BP in the presence of an acute onset of end organ dysfunction (e.g., renal failure,
encephalopathy, papilledema).
Prognosis:
prolonged excessive BPs are associated with high rates of CAD, stroke, CHF, and renal failure;
excessive decreases in BP can lead to organ hypo perfusion.
{In a hypertensive emergency (give IV med) the initial decrease in DBP should not exceed 25% of the
presenting pressure to avoid triggering an ischemic event}.
{Reduce the diastolic BP to 100 mm Hg using IV nitroprusside, labetalol, or fenoldopam.
After the initial reduction use oral β-blocker and ACE-I to maintain mean DBP at 100 to 105 mm Hg}.
Thoracic aortic aneurysms (TAA) Risk factors:
Atherosclerosis* (HTN, Hyperlipidemia)
Smoking
Age>60yrs, white race and family history
Marfan syndrome, Ehler danlos syndrome and Syphilis => Causes more TAA than AAA
(The most important modifiable risk to prevent worsening of existing aneurysms is uncontrolled
Hypertension).
4
[Diseases Risk factors/Prognosis/Mnemonics for USMLE STEP 3]
Sources used: MTB 2, MTB 3, MTB IM, FA 3, Step Up to Medicine, Step Up to Step 3
Cardiology
Coronary Artery Disease Risk Factors:
The most clearly agreed-upon risk factors for CAD are:
Diabetes mellitus
Tobacco smoking
Hypertension
Hyperlipidemia
Family history of premature coronary artery disease (Men 55 years; women 65 years)
Age above 45 in men and above 55 in women
The worst risk factor for CAD is diabetes mellitus, but the most common risk is hypertension.
{Common risk factors for atherosclerosis may be remembered by the mnemonic SHIFT MAID: Smoking,
HTN, Insulin resistance (NIDDM), Family history, Triglycerides and cholesterol (high), Male, Age
(increased), Inactivity, Diet}.
Less Reliable but Probable Risk Factors for CAD:
Physical inactivity
Excess alcohol ingestion
Insufficient fruits and vegetables in the diet
Emotional stress
Elevated cardiac CT scan calcium scores
Positron emission tomography (PET) scanning
Increased physical activity and exercise reliably lower all-cause mortality, but physical inactivity is
not as severe a risk for coronary disease as diabetes and hypertension
Calcium scores on a CT scan of the heart are still considered experimental. It is not clear what to do
differently with this information in addition to standard risk factors.
Unreliable (Unproven) Risk Factors for CAD:
Several disease markers such as elevated homocysteine levels, chlamydia infection, and elevated C
reactive protein levels have not proven to be reliable. There is no benefit to measuring, following, or
attempting to therapeutically intervene on these factors.
1
,CAD can have the following clinical presentations:
• Asymptomatic
• Stable angina pectoris
• USA pectoris
• MI—either NSTEMI or
STEMI
• Sudden cardiac death
Prognostic indicators of CAD:
a. Left ventricular function (ejection fraction [EF])
• Normal 50%
• If <50%, associated with increased mortality
b. Vessel(s) involved (severity/extent of ischemia)
• Left main coronary artery—poor prognosis because it covers approximately two-thirds of the heart
• Two- or three-vessel CAD—worse prognosis
{Stable angina prognosis
Is related to the ability to prevent progression of atherosclerosis and to control comorbid factors; left
ventricle function and the degree of left coronary artery occlusion are the strongest predictors of long-
term survival}.
{Unstable angina prognosis
Short-term prognosis is frequently predicted by the thrombolysis in myocardial infarction (TIMI) risk
score.
Long-term prognosis is best predicted by EF and the degree of residual ischemia detected on
posttherapy stress testing.
Up to 10% of patients will have a myocardial infarction or will die within 6 months following the onset of
new unstable angina.
One third of patients will have a myocardial infarction within 3 years after a new onset of unstable
angina}.
{MI Prognosis
there is a 30% acute mortality with 50% of survivors being rehospitalized within 1 year and 10% dying
within 1 year; complications include infarct extension, arrhythmias, myocardial dysfunction, papillary
muscle necrosis, wall rupture, aneurysm, mural thrombus, pericarditis, and Dressler syndrome (i.e.,
fever, pericarditis, and increased erythrocyte sedimentation rate [ESR] 2 to 4 weeks post-MI)}.
{The differential diagnosis for chest pain may be remembered by the mnemonic
CHEST PAIN: Cocaine/Costochondritis, Hyperventilation/ Herpes zoster, Esophagitis/
Esophageal spasm, Stenosis of aorta, Trauma, Pulmonary embolism/ Pneumonia/
Pericarditis/Pancreatitis, Angina/ Aortic dissection/ Aortic aneurysm, Infarction (myocardial),
Neuropsychiatric disease (depression)}.
{Treatment for MI may be remembered by the mnemonic Be MONA: Beta-blocker,
Morphine, O2, Nitroglycerin, ASA/ ACE-I}.
2
,CHF Risk factors:
CAD
HTN
valvular disease
cardiomyopathy
COPD
drug toxicity
alcohol use
{CHF due to systolic dysfunction
First medications given are typically loop diuretics (decrease heart preload) and either ACE-I or
angiotensin receptor blockers (ARB) (decrease preload and afterload and increase cardiac output).
β-blockers may be added once a stable ACE-I dose is prescribed and should not be administered during
acute exacerbations.
Digoxin (increases contractility) may be added to the regimen to improve symptoms but has not
demonstrated an ability to improve mortality.
Spironolactone or vasodilators may be added for persistent symptoms.
CHF due to diastolic dysfunction
BP is controlled with calcium channel blockers, ACE-I, or ARB.
β-blockers are useful to control the heart rate and to decrease cardiac workload in stabilized patients.
K-sparing diuretics should be given to reduce cardiac hypertrophy caused by aldosterone.
Recombinant BNP (i.e., nesiritide) has been shown to improve outcomes during severe acute
exacerbations.
Underlying conditions should be treated.
The patient should adhere to a low-salt diet.
Progressive cases may require cardiac transplant or implantation of an assistive device (indicated for an
ejection fraction below 35%)}.
{Frequent causes of CHF exacerbations are remembered by the mnemonic A SMITH
PEAR: Anemia, Salt, MI, Infection, Thyroid (high or low), HTN, Pericarditis, Endocarditis, Arrhythmia, Rx
(not taking medications)}.
CHF Prognosis:
Approximately half of patients with CHF will eventually die from a ventricular arrhythmia.
Hospital admission is associated with up to a 20% mortality rate.
Mortality increases to 40% in the presence of a comorbid MI and 80% in the presence of hypotension.
Hyperlipidemia Risk factors:
a. Diet
• Saturated fatty acids and cholesterol cause elevation in LDL and total cholesterol
• High-calorie diets do not increase LDL or cholesterol levels (are “neutral”)
but do increase triglyceride (TG) levels
• Alcohol increases TG levels and HDL levels but does not affect total cholesterol levels
b. Age—cholesterol levels increase with age until approximately age 65. The increase is greatest during
early adulthood—about 2 mg/dL per year
c. Inactive lifestyle, abdominal obesity
d. Family history of hyperlipidemia
3
, e. Gender—men generally have higher cholesterol levels than do women; when women reach
menopause, cholesterol levels then equalize and may even be higher in women than in men
f. Medications
• Thiazides—increase LDL, total cholesterol, TG (VLDL) levels
• β-Blockers (propranolol)—increase TGs (VLDL) and lower HDL levels
• Estrogens—TG levels may further increase in patients with hypertriglyceridemia
• Corticosteroids and HIV protease inhibitors can elevate serum lipids
g. Genetic mutations that predispose to the most severe hyperlipidemias
h. Secondary causes of dyslipidemia
Hypertension Risk factors:
Age—both systolic and diastolic BP increase with age.
Gender—more common in men (gap narrows over age 60); men have higher complication rates.
Race—it is twice as common in African-American patients than in Caucasian patients; African-American
patients also have higher complication rates (stroke, renal failure, heart disease).
Obesity, sedentary lifestyle, dyslipidemia.
Family history.
Increased sodium intake—this correlates with increased prevalence in large populations, although not in
individuals; individual susceptibility to the effects of high salt intake varies.
Alcohol—intake of more than 2 oz (8 oz of wine or 24 oz of beer) per day is associated with HTN.
Prognosis:
Untreated or poorly treated disease increases the risk of CAD, stroke, aortic aneurysm, aortic dissection,
CHF, kidney disease, and ophthalmologic disease.
Long-term prognosis is directly related to the ability to control BP, ability to reduce unhealthy behaviors,
and the avoidance of complications.
The behaviors that are risk factors for HTN are also associated with diabetes mellitus.
Hypertensive emergency:
Excessive BP in the presence of an acute onset of end organ dysfunction (e.g., renal failure,
encephalopathy, papilledema).
Prognosis:
prolonged excessive BPs are associated with high rates of CAD, stroke, CHF, and renal failure;
excessive decreases in BP can lead to organ hypo perfusion.
{In a hypertensive emergency (give IV med) the initial decrease in DBP should not exceed 25% of the
presenting pressure to avoid triggering an ischemic event}.
{Reduce the diastolic BP to 100 mm Hg using IV nitroprusside, labetalol, or fenoldopam.
After the initial reduction use oral β-blocker and ACE-I to maintain mean DBP at 100 to 105 mm Hg}.
Thoracic aortic aneurysms (TAA) Risk factors:
Atherosclerosis* (HTN, Hyperlipidemia)
Smoking
Age>60yrs, white race and family history
Marfan syndrome, Ehler danlos syndrome and Syphilis => Causes more TAA than AAA
(The most important modifiable risk to prevent worsening of existing aneurysms is uncontrolled
Hypertension).
4
