Angina Pectoris

Angina is the sensation caused by the myocardial ischemia that result when cardic metabolic demand exceeds supplu. Its
generally defined as pressure, discomfort, or a choking sensation in the left ches that is precipitated by exertion,
excitement, or cold weather, and relieved by rest or nitroglycerin. In some patients, the discomfort radiates into the left
arm, into the jaw, or more rarely, into the right arm. When severe, it can be accompanied by dyspnea, diaphoresis, or
nausea. Not all patients experienceese classic symptoms, and in some individuals myocardial ischemia may acause
atypical symptoms such as jaw pain, fatigue, arm discomfort, or upper abdominal pain. Myocardial ischemia can also be
silent (not associated with symptoms), especially in diabetic patient.

Etiology

The most common caue of angina is obstruction of coronary arteries by atherosclerosis. Risk facors include
hypertension, tobbaco use, diabetes mellitus type 1, diabetes mellitus type 2, hypercholestrolemia, and family history of
premature vascular disease.

Clinical Presentation

CAD generally manifests as chronic stable angina, unstable angina, acute myocardial infarction, unrecognized myocardial
infarction, or sudden cardiac death. Patients with acute myocardial infarction can be further subdivided into those with
ST elevation on electrocardiogram (ECG) and those without ( commonly called non-ST elevation myocardial infarction).

1. Chronic stable angina

Fixed, stable, obstructive CAD causes a syndrome termed chronic stable angina that occurs when myocardial
metabolic demand exceeds a fixed treshold of supply. Angina is commonly precipitated by exertion, emotional
excitement, mental stress, or exposure to cold, and resolves after precipitating event has ceased. Angina
generally occurs at the same level of exertion but may vary depending on time of the day, recent meals, and
ambient temperature.
The most used classification for grading angina severity is the Canadian Cardiovascular Society scale. Patients in
Class I experience angina with strenous or protracted physical activity, whereas those in Class II occasionally
have angina with normal daily activities such as climbing stairs or walking up a hill. Patients in Class III have
marked limitation and commonly experience angina during activities of everyday living ( e.g. walking across a
room). Clas IV symptoms occur at rest.
2. Unstable angina or Non-ST elevation myocrdial infarction
Unstable angina, pr non-ST elevation myocardial infarction, is generally die to formation of a nonocclusive
thrombus at the site rupture or erosion t=of the surface of an atheroslerosis plaque. This event exposes the
blood to the highly thrombotic materials within the plaque, leading to thrombus formation. Te thrombus can
progress until it occludes the blood vessel or, alternatively, may embolize and occlude smaller, distal vessels.
Sudden onset of chest discomfort that is unrelated to a precipitating event is a hallmark of this syndrome.
3. Actute myocardial infarction with ST segment elevation
Acute STEMI is characterized by the abrupt onset of unremitting chest discomfort and is generally associated
with dyspnea, diaphoresis, and a sense of doom. It is typically caused by abrupt occlusion of a coronary artery
by thrombus at the site of a ruptured atheroslerotic plaque. The ECG shows ST elevation in two or more leads
corresponding to the territory of a coronary artery. Patiens who are not treated within 6 to 2 hours generally
suffer sign ificantmyocardial damage.

Diagnostic Approach

1. Chronic stable angina

 In chronic stable angina, typical history and presence of risk factor are the most important information for
diagnosis. The physical examinination usually not helpful but may provide evidence of left ventricular systolic or
diastolic disfunction (S3 or S4 respectively). During an attack of angina, patients tend to be still and may apear
pale. The ECG is normal in more than half of patients with atheroslerosis, but there may be evidence of prior
myocardial infarction or ischemia (e.g. ST deppression). The three most important determinants of prognosis in
patients with chronic stable angina are age, number of diseased coronary arteries, and left ventricular function.

An exercise treadmill test can diagnose CAD by the development of ECG changes with exercise. in addition
symptoms during exercise, blood pressure response, and duration of exercise are all important in determining
the post-test probability of CAD and whether the patient needs further evaluation. The treadmill test can be
enhanced by assessing left ventricular wall motion (with echocardiography) or myocardial perfusion (with
nuclear imaging). Pharmacologic stress testing can be used in patients who are unable to exercise.
The recent advent of 64-slice computed tomography C 1) Scanners has enabled noninvasive coronary
angiography. Patients are given an intravenous bolus of contrast dye, and then the coronary arteries are
imaged. The use- fulness of this test remains to be determined, but there are promising data, especially in
excluding CAD in low-risk patients. CT angiography has several limitations, including significant radiation
exposure, exposure to contrast Dye, the need to be in sinus rhythm, and an ability to tolerate relative
bradycardia.
Direct coronary angiography remains the gold standard for diagnosing CAD. This test, which involves direct
injection of contrast dye into the coronary arteries, delineates the location and severity of obstructive coronary
disease. 60 As such, angiography is a necessary prerequisite for coronary disease revascularization through
either percutaneous ov intervention or coronary artery bypass surgery. Left ventriculography, generally
performed immediately before or after coronary angiography, provides important information regarding
intracardiac pressures and left ventricular function.
Clinically assessing the functional importance of intermediate lesions (lesions that appear to obstruct 40% to
60% of the coronary lumen) may be difficult using coronary angiography alone. This limitation can be partially
overcome by using intracoronary ultrasound or by mea en- suring coronary flow velocity or intracoronary
pressure or changes during maximal hyperemia

2. Acute coronary syndromes

Patients with unstable angina, non-ST elevation myocardial infarction, or ST elevation myocardial infarction are
considered to have an acute coronary syndrome. The diagnosis is generally based on constellation of typical
symptoms, ECG changes, and elevated levels of cardiac enzymes ( in the caze of myocardial infarction )
3. Actute myocardial infarction with ST segment elevation
Highly sensitive blood test for myocardial proteins have greatly enhanced our abitily to diagnose myocardial
infarction. Troponins and creatinine kinase-MB (CK-MB) are intercellular cardiac proteins released into the
bloodstream upon the the death pf myocytes. Plasma levels of these proteins are useful both in detecting
myocardial infarction and establishing prognosis. Troponin and CK-MB do not appear in plasma in significant
levels until 8 or more hours after the onset of symptoms, limiting their diagnostic value in the very early stages
of actute coronary syndromes.

Management and Therapy

1. Nonpharmacologic Interventions
Patients should be advised on the need to lower the intake of cholesterol and satureated fat in their diets, the
importance of weight loss if obese, and the need to avoid tobacco. A regular excercise program should be
 prescribed for all patients in whom it is feasible. An excercise test can be used to determine safe levels of
activity.
2. Pharmachologic interventions
Pharmacological therapy for angina was traditionally direcyed at relieveing symptoms. More recently,
medications have been classified based on their effect on survival. Medications that improve survival and
decrease cardiovacular events in patients with CAD incluse aspirin, hydroxymethyl glutaryl-coenzyme (HMG-
CoA), reductase inhibitor (station) and angiotensin-converting enzyme inhibitor. In patients with myocardial
infarction or left ventricular dysfunction, -Blokers also reduce mortality. Medications that treat symptoms
without improving survival include nitrates and calcium channel blokers.
Low density lipoprotein (LDL) cholesterol levels should be agressively lowered, even in patients with ostensibly
normal LDL levels, trough the use of diet and statins. Recent guidelines suggest that LDL sholesterol should be
less than 70 mg/dL in patients with CAD. Blood pressure should be closesly monitored, with optimum levels
below 140/90 mmHg. In diabetic patients, optimum levels are even lower, with the goal of diastolic blood
pressures at 80 mmHg or less.
In ST elevation myocardial infarction, the goal od therapy is rapid restoration of blood flow using either
thrombolitic therapy or a percutaneous coronary intervention such as balloon angioplasty.
3. Revascularization
Revascularization re-restablishes unobstructed blood flow either trough percutaneous intervention, in which
the athereosclerotic blockage is relieved by angioplasty balloon inflation or stent placement, or by coronary
artery bypass in grafting, in which blood flow is diverted around atherosclerotic obstruction using an arterial (
e.g left internal mammary artery) or venous conduit. Revascularization prolongs survival in parients
withsignificant left main CAD and multivessel CAD with impaired left ventricular function. The most common
indication for revascularization is to relieve the symptoms.

Avoiding treatment errors

One of the most common, major, preventable treatment errors is the misdiagnosed of acute myocardial infarction.
Another major problem to avoid is the undertreatment of ST elevation myocardial infarction.

Future Directions
Plasma levels of C-reactive protein, a marker of inflammation are useful in determining the prognosis or patients
with unstable angina or non-ST elevation myocardial infarction.
__________________________________________________________________________________________________

DIABETES AND PREDIABETES DIAGNOSIS AND TREATMENT 291

Introduction
DM is a major cause of morbidity and mortality. Premature vascular disease is the eventual cause of death in more than
two thirds of people with DM, leasing to a loss more than 10 years of life in those diagnosed ad age 40 years.
Type 2 DM generally occurs in adulthood, although it can develop at any age. Currently, almost half of children with
new-onset diabetes now have type 2 diabetes. Most of patients with type 2 DM have a first-degree relaive with DM, and
most are pverweight,generally with a central pattern of obesity. From recent prospective studies, type 2 DM develops as
the result of progressive loss of insulin secretory capacity on the background of insulin resistance.
Clinical presentation
In type 2 DM, patients may be completely asymptomatic for years. Some present with classic symptoms of
microvaskular or macrovaskular complications. More often, subtle symptoms may be present for years, including
fatigue, reccurent cutaneous infections, and intermittent nocturia. If hyperglycemia is allowed to progress uncheked,
life-thretening problems can develop.
Diagnostic approach
About two third of cases od DM in the United States are undiagnosed. In some studies, 20% to 50% people with DM
have one or more complications of the disease at the time that a diagnosis is made.
Current recommendations suggest screning for DM by measuring a fasting plasma glucose (FPG) starting at age 45 years,
with repeat screening every 3 years. Screening should start at early age and be repeated at shorter intervals,
particularly in people who are overweight with one or more risk factors :
- A family history of FM in a first-degree relative
- Belonging to a high-risk etnhic group
- Hypertension
- Dyslipidemia ( high trygliserides or low HDL)
- Women with history of gestational diabetes, birth of a child greater than 9 pounds, or ovarium
hyperandrogenism
-Prior abnormal fasting glucose or tolerance test
- Acanthosis nigirican
- Known vascular disease
Normal levels of glucose are defined as follows :
-Fasting < 100 mg/dL
- 2 hout OGTT < 140 mg/dL
The following glevels of glucose are suggestive of diabetes but requiere confirmation for diagnosis
-Fasting > 126 mg/dL
-2-hour OGTT 200 mg/dL
- In patients with symptoms of diabetes ( polyuria, polydipsia, weight loss, random glucose measerements > 200
mg/dL
Generally to make the diagnosis, measurements should be made on 2 separate days either repeating the same test or
performing another.
Management and therapies PAGE 294-7
PREVENTION AND TREATMENT OF COMPLICATIONS OF DIABETES

Etiology and pathogenesis

Glucose-dependent mechanism for the development of complications have been described, including the intracellular
accumulation of sorbitol, overativity of protein kinase C, and the development of advanced glycostation end product.
With respect to both CVD and microvascular complications, the contribution or hyperglycemia, increased blood
pressure, lipid disorder, hypercoagulability, and smoking is absolutely clear.
Clinical presentation
With regard to microvascular disease, the classic presentations of angina, myocardial infarction, stroke, transient
ischemic attacks, and claudication are quite common. A recent study documented that among patients with type 2
diabetes between the ages of 50 to 75 years who had no history of ischemic heart disease, a normal electrocardiogram,
and negative screening quistionnare for anginal symptomps, 22% had silent ischemiia by elektrocardiograph (ECG)-
gated adenosine-stress single-photoon emission computed tomography.
Diagnostic approach
The key to management of the complications of diabetes is screening to detect early manifestations. For CVD, relevant
recommendations include the following :
Blood pressure should be measured at every visit. If the blood pressure is 130 mmg or greater sistolic, or 80
mmHg or greater diastolic, the elevation should be confirmed on separate day.
A fasting lipid panel should be performed anually. If the patient is not available for testing in the fasting state, a
nonfasting non-high-dnsity lipoprotein (non-HDL) cholesterol is a reasonable surrogate for low-density
 lipoprotein (LDL) cholesterol but may miss even severe disoerders of HDL or tryglyceride metabolism. If the full
fasting lipid panel is normal, testing may be deferred to every 2 years.
Diagnostic stress testing with imaging procedures should be considered in those with ECG abnormalities, typical
or atypical cardiac symptoms, known as vascular disease or sedentary lifestyly older than 35 years who are
planning to start vigorous exercise program. Routine stress testing will identify many patients with disease, but
it remains unclear wether invasive management is associated with improved outcomes in the setting of
asymptomatic CVD in diabete.

Management
Because more than two thirds of patients with DM die from CVD, agressive management of other cardiovascular risk
factors at least as important as glucose management. Current recomendations suggest that most patients with DM
should do teh following :
Take aspurun 81 mg/day (if older than 40 years or older than 30 years with additional CVD factors)
Reduce blood pressure to less than 130/80 mmHg with a blood pressure regimen that generally includes
angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor bloker (ARB)
Take a statin at a dose adequate to reduce LDL cholesterol by 30% to 40% and to reduce LDL to less than 100
mg/dL (<70 mg/dL in the setting of CVD)
Reduce triglycerides to less thn 150 mg/dL
Stop smoking or dont start.
Avoiding treatment errors
The most common errrors in the management of diabetic complications are failure to make a timely diagnosis and
nonadherence to treatment guidelines once a diagnosis is made, often as a result of oversight. The health care team
(both patients and providers) should keep a checklist to ensure that all the listed screeningn test are performed at least
anually and recommended preventative therapies continued.

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1. Runge MS, Greganti MA, Netter FH. Netters internal medicine. 2nd ed. Philadelphia: Saunders/Elsevier;
2009.p 186-301.