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Cardiovascular Disease

 

Cardiovascular Disease

·        Cardiovascular Disease = leading cause of death in the U.S., surpassing cancer and respiratory disease

·        Risk factors for Cardiovascular Disease

o       Age: most powerful independent risk factor; men >55 y/o, women >65 y/o have increased risk

o       Family history of premature Cardiovascular Disease (e.g., Hypertension, hyperlipidemia, Diabetes Mellitus)

o       Hypertension

o       Tobacco

o       Hyperlipidemia (increased LDL, increased triglycerides, decreased HDL)

o       Diabetes Mellitus: Dr. Gerula emphasized that if a patient has Diabetes Mellitus, their risk for an MI is the same as a person who does not have Diabetes Mellitus but who has had a previous Myocardial Infarction

o       Sedentary lifestyle

o       Obesity

o       Heavy alcohol usage (moderate use may increase HDL = good)

o       Biological markers: increased CRP (c-reactive protein), increased urine microalbumin (destruction of renal blood vessels can compromise the filtering ability of kidney, leading to microalbumin leaking into urine; indicative of systemic arterial damage)

·        Normally, vasodilation occurs with increased usage and vasoconstriction occurs at rest; atherosclerosis causes hardening of these arteries, preventing this normal reaction

 

Types of Cardiovascular Disease

Stable Angina (Angina Pectoris)

·        Predictable and reproducible; obstruction takes years to progress; often in elderly
·
           

 
Stable plaque burden (i.e., >70% of vessel is occluded); the greater the occlusion, the greater likelihood that the plaque will be stable and NOT rupture (compare with acute coronary syndrome that has a smaller plaque burden and is more likely to cause an MI)

Blood/oxygen supply ¹ body’s demand for blood/oxygen upon exertion

Clinical presentation: 72 y/o male, PMHx: Diabeters Mellitus, Hypertension, high cholesterol; complains of shortness of breath and chest heaviness after climbing two flights of stairs; symptoms resolve after resting for 5 minutes; does not experience these chest pains when walking on flat ground; sometimes gets pain that extends to lower jaw and radiates down left arm; symptoms have lasted for a few months
 

 

·        Diagnosis

o       EKG: may be normal, show evidence of an old MI, or may have T-wave inversion

o       Angiogram: thread a catheter from femoral artery > aorta > aortic arch, inject radioactive contrast, and assess perfusion by x-ray

o       Stress test

§         Increase cardiac demands on patient either by administering drugs or by increasing intensity of exercise activity (i.e., treadmill), and see at what point cardiac symptoms are reproduced

§         Assess via echocardiogram (realtime video of heart wall in motion)

·        Treatment

o       Nitrates: sublingual administration leads to systemic and coronary artery vasodilation

o       b-blockers or calcium-channel blockers: decrease heart rate, contractility, and blood pressure

o       Coronary intervention: insert a stent into occluded artery to increase blood flow; must also take aspirin/PlavixÒ (anti-platelet drugs) for 6-9mos while artery is healing

 

Acute Coronary Syndrome

·        Clinical presentation:

o       Patient from before (72 y/o male who had stable angina) now comes into your office complaining that for the past 2 days, he has been unable to walk up 1 flight of stairs without having shortness of breath, and has been experiencing more severe chest pain than before

o       Or… 42 y/o male with a history of Hypertension and tobacco use complains of chest pain starting last night.  Patient has a family history of Coronary Artery Disease.

o       Patients generally present with rapidly-worsening chest pain (i.e., over the past few hours/days) after minimal exertion or even at rest; chest pain is very severe

·        Acute coronary syndrome progression:

  1. Unstable plaque (with fibrous cap) forms; in contrast to stable angina that has highly-occlusive plaques, acute coronary syndrome includes plaques that occlude less than 50% of the vessel; these smaller, more immature plaques lead to Myocardial Infarction’s
  2. Fibrous plaque ruptures, lipid core is exposed, and lipids (LDL) spill out into circulation
  3. A “dance” then ensues (not unlike Elaine’s memorable arm/leg-jerking dance on Seinfeld) between thrombosis and thrombolysis, with thrombosis typically winning out

·        Types of Acute Coronary Syndrome:

1.      Unstable Angina

·        Ischemia but NO infarction; “heart muscle is being choked, but not killed”

·        EKG: normal, deep T-wave inversion, or ST-depression

·        Do NOT see presence of cardiac enzymes that suggest infarction (CPK-MB, troponins)

2.      Non-ST Elevation Myocardial Infarction (NSTEMI)

·        Ischemia AND infarction

·        EKG: normal, deep T-wave inversion, or ST-depression

·        DO see the presence of CPK-MB and troponins

3.      ST Elevation Myocardial Infarction (STEMI)

·        Ischemia AND infarction

·        EKG: see ST-elevation or Left Bundle Branch Block

·        DO see the presence of CPK-MB and troponins


·        Acute Management of Acute Coronary Syndrome

o       Provide oxygen to address oxygen supply/demand imbalance

o       Anticoagulants (heparin)

o       b-blockers

o       Antiplatelets (aspirin or clopidogrel—PlavixÒ)

o       Thrombolytics (used in STEMI)

o       Mechanical (stents, coronary artery bypass graft)


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