2-variant angina or Prinzmetal angina

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• 2-variant angina or Prinzmetal angina
• - Is angina occurring at rest due to coronary
  artery spasm.
• - completely normal vessels can be affected.
• - Treatment administration of vasodilators such
  as nitroglycerin or calcium channel blockers.

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• 3-Unstable angina (also called crescendo angina)
• - occurring with progressively less exertion or
  even at rest.
• a fixed 90 stenosis can lead to inadequate
  coronary blood flow even at rest.

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• characterized by increasing frequency of pain,
  precipitated by progressively less exertion.
• the episodes also tend to be more intense and
  longer lasting than stable angina
• ? called pre-infarction angina
• associated with plaque disruption
  superimposed partial thrombosis

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Myocardial Infarction

• - Popularly called heart attack is necrosis of
  heart muscles resulting from ischemia
• Pathogenesis
• Most cases of MI are caused by acute coronary
  artery occlusive thrombus
• In most cases, disruption of atherosclerotic
  plaque results in the formation of thrombus

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Clinical manifesataions

• 1) Severe, crushing substernal chest pain
• 2) Discomfort that can radiate to the neck, jaw,
  epigastrium, or left arm.
• MI? pain lasts from 20 minutes to several hours
  and is not relieved by nitroglycerin or rest.

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• - Myocardial infarction can be entirely
  asymptomatic in 10 to 15 of the cases (silent
  infarcts)? particularly common in patients with
  underlying diabetes mellitus (with peripheral
  neuropathies)

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• 4. The pulse is rapid and weak
• 5- Nausea
• 6- Dyspnea is common (impaired myocardial
  contractility and dysfunction of the mitral valve
  apparatus, with resultant pulmonary congestion
  and edema).

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Lab evaluation of MI

• Is based on evaluation of blood levels
  macromolecules that leak out through damaged cell
  membranes , include myoglobin, Creatin kinase-MB,
  Troponin T and I.
• 1. Total CK is not reliable marker for cardiac
  injury

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• 2. Ck-MB remains a valuable marker of myocardial
  injury second only to cardiac specific troponins.
• It begins to rise within2-4 hours, peaks at 24-48
  hours, and return back to normal within 72 hours

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• 3. Troponin T and I (Tnt and Tni)
• After MI , both are detectable within 2-4 hors
  and peak at 48 hours and remain elevated for 7 to
  10 days

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• - The frequencies of involvement of each of the
  three main arterial trunks are as follows
• Left anterior descending coronary artery (40
  to 50)
• infarcts involving the anterior wall of left
  ventricle
• the anterior portion of ventricular septum
• and the apex circumferentially

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• 2. Right coronary artery (30 to 40) infarcts
  involving the
• Inferior/posterior wall of left ventricle
• posterior portion of ventricular septum
• and the inferior/posterior right ventricular free
  wall in some cases

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• 3. Left circumflex coronary artery (15 to 20)
• - Infarcts involving the lateral wall of left
  ventricle except at the apex

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• Complications following acute MI
• 1 Contractile dysfunction.
• There is usually some degree of left ventricular
  failure with hypotension, pulmonary vascular
  congestion, which can progress to pulmonary
  edema

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• 2. Arrhythmias.
• Many patients have myocardial irritability and/or
  conduction disturbances following MI that lead
  to potentially fatal arrhythmias such as
  ventricular fibrillation
• The risk of arrhythmias is greatest in the first
  hour after MI

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• 3. Myocardial rupture. Most commonly occur within
  2-4 days
• These include
• a. Rupture of the ventricular free wall (most
  common), with hemopericardium and cardiac
  tamponade
• b. Rupture of the ventricular septum (less
  common), leading left-to-right shunting

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• 4- Mural thrombus.
• - With any infarct, the combination of a local
  abnormality in contractility (causing stasis) and
  endocardial damage (creating a thrombogenic
  surface) can foster mural thrombosis and
  potentially thromboembolism.

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• 5.Ventricular aneurysm.
• Aneurysms of the ventricular wall are a late
  complication of large transmural infarcts
• - Complications of ventricular aneurysms include
  mural thrombus,
• - Rupture of the tough fibrotic wall does not
  usually occur.

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Infective endocarditis

• - Is a microbial infection of the heart valves or
  endocardium that leads to the formation of
  vegetations composed of thrombotic debris and
  organisms, often associated with destruction of
  the underlying cardiac tissues.

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• I. Acute infective endocarditis
• a. Is typically caused by infection of a
  previously normal heart valve by a highly
  virulent organism (e.g., Staphylococcus aureus)
• b. That rapidly produces necrotizing and
  destructive lesions.

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• c- These infections may be difficult to cure
  with antibiotics alone, and usually require
  surgery.
• d- Despite appropriate treatment, death can
  ensue within days to weeks.

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• 2.Subacute IE is characterized by
• a. organisms with lower virulence (e.g.,
  streptoccocus viridans )
• b. cause insidious infections of deformed valves

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• c. Less destruction.
• d. The disease may pursue a protracted course of
  weeks to months, and cures can be achieved with
  antibiotics.

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• Note
• - Endocarditis of native but previously damaged
  or otherwise abnormal valves is caused most
  commonly (50 to 60 of cases) by Streptococcus
  viridans, a normal component of the oral cavity
  flora.

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• In contrast, more virulent S. aureus organisms
  commonly found on the skin can infect either
  healthy or deformed valves and are responsible
  for 20 to 30 of cases overall
• S. aureus is the major offender in IE among
  intravenous drug abusers

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• The source may be
• a. an obvious infection elsewhere,
• b. a dental or surgical procedure,
• c. a contaminated needle shared by intravenous
  drug users, or
• d. seemingly trivial breaks in the epithelial
  barriers of the gut, oral cavity, or skin.

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• In patients with valve abnormalities, or with
  known bacteremia, IE risk can be lowered by
  antibiotic prophylaxis.