1. Ischemic Heart Disease
Hisham Alkhalidi

3. Ischemic Heart Disease
A group of related syndromes resulting from myocardial ischemia
Ischemia is an imbalance between cardiac blood supply (perfusion) and myocardial oxygen demand
ischemia can result from increased demand (e.g., increased heart rate or hypertension)
diminished oxygen-carrying capacity (e.g., anemia, carbon monoxide poisoning)

4. Ischemic Heart Disease
The vast majority of ischemic heart disease is due to coronary artery atherosclerosis
Less frequent contributions of:
vasospasm
vasculitis
Is it exactly the same as coronary artery disease (CAD)?
Frequently yes
in the vast majority of cases, IHD is due to a reduction in coronary blood flow caused by obstructive atherosclerotic disease
Thus, IHD is also frequently called coronary artery disease (CAD).

5. Plaque disruption= fissure, ulceration or rupture
Plaques with large atheromatous core or those in which the overlying fibrous caps are thin are more likely to rupture and are therefore denoted as "vulnerable.“
Fissures frequently occur at the junction of the fibrous cap and the adjacent normal plaque-free arterial segment, a location at which the mechanical stresses are highest and the fibrous cap is thinnest. Fibrous caps are also continuously remodeling; the balance of collagen synthesis and degradation determines its mechanical strength and thus plaque stability
Vasospasm and/or platelet aggregation can contribute but are infrequently the sole cause of an occlusion

7. Ischemic Heart Disease Angina pectoris
Chest pain:
Can radiate down the left arm or to the left jaw (referred pain)
Due to inadequate perfusion
Duration and severity is not sufficient for infarction

8. Ischemic Heart Disease Stable angina
Occurring reliably after certain levels of exertion
Typically due to atherosclerotic disease with ≥75% (critical stenosis) fixed chronic stable stenosis
Nitroglycerin, by reducing the venous return, large doses-> increase blood to heart
Regrettably, it is presently impossible to reliably predict plaque rupture in any given patient

9. Ischemic Heart Disease Unstable angina
Unstable (occurring with progressively less exertion or even at rest)
Results from a small fissure or rupture of atherosclerotic plaque triggering:
Platelet aggregation
Vasoconstriction
Formation of a mural thrombus that may not be occlusive
Usually proceed MI
crescendo

10. Ischemic Heart Disease Variant angina
Vessel spasm or Prinzmetal angina
Without fixed atherosclerotic disease
The etiology is not clear
Responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers

12. Ischemic Heart Disease Myocardial infarction
The severity or duration of ischemia is enough to cause cardiac muscle death
Typically results from acute thromboses that follow plaque disruption

14. if a coronary artery develops atherosclerotic occlusion at a sufficiently slow rate, it may be able to stimulate collateral blood flow from other major epicardial vessels; such collateral perfusion can then protect against MI even in the setting of a complete vascular occlusion. Unfortunately, acute coronary occlusions cannot spontaneously recruit collateral flow and will result in infarction
Influences extrinsic to the plaque are also important. Adrenergic stimulation can elevate physical stresses on the plaque through systemic hypertension or local vasospasm. Indeed, the adrenergic stimulation associated with awakening and rising may underlie the known peak incidence (between 6 am and 12 noon) of acute MIs. Intense emotional stress can also contribute to plaque disruption.

15. Ischemic Heart Disease MI types
Transmural
Full thickness (>50% of the wall)
Subendocardial
Inner 1/3 of myocardium
Two mechanisms:
Fixed atherosclerosis but with increased demand, vasospasm or hypotension OR
Evolving transmural with relieve of the obstruction (often multifocal)
Transmural , sever coronary atherosclerosis with acute plaque rupture and superimposed thrombosis

16. Ischemic Heart Disease MI, common locations
In Right dominant coronary artery heart (90% of population):
2 cm proximal LAD (up to 50%)
anterior left ventricle
anterior septum
apex circumferentially
Left circumflex ( up to 20%)
infarct involves lateral left ventricle except the apex
1st and last thirds of RCA (up to 40%)
posterior left ventricle
posterior septum
right ventricular free wall, sometime
Mostly LV, 15% with right ventricle
You have to know basic anatomy
Septal , posterior part supplied by posterior septal is provided by the dominant artery

23. Within seconds of vascular obstruction, cardiac myocyte aerobic glycolysis ceases, leading to inadequate production of adenosine triphosphate (ATP) and accumulation of potentially noxious breakdown products (e.g., lactic acid).
Ischemia to myocardium rapidly (minutes) leads to loss of function and causes necrosis after 20 to 40 minutes

24. Ischemic Heart Disease
Ischemia to myocardium rapidly (minutes) leads to loss of function and causes necrosis after 20 to 40 minutes
VASOspasm and platelet aggregation lead to MI without athersclerosis
that an infarct usually reaches its full size within 3 to 6 hours. Any intervention in this time frame can potentially limit the final extent of necrosis

25. If patient survive thrombi may lyse spontaneous or by rx
Or vasospasm relief , reestablish the flow
of reperfusion injury that can incite greater local damage than might have otherwise occurred without rapid restoration of blood flow. reperfusion injury is mediated in part by oxygen free radicals generated by the increased number of infiltrating leukocytes facilitated by reperfusion. Reperfusion-induced microvascular injury causes not only hemorrhage but also endothelial swelling that occludes capillaries and may prevent local blood flow (called no-reflow).
A reperfused infarct usually has hemorrhage because the vasculature injured during the period of ischemia is leaky after flow is restored

26. Ischemic Heart Disease Clinical picture of MI
Severe, crushing substernal chest pain or discomfort that can radiate to the neck, jaw, epigastrium, or left arm
Diaphoresis
Nausea
Dyspnea
Can be silent (DM, old age)
Diaphoresis is excessive sweating commonly associated with shock and other medical emergency conditions.

27. Ischemic Heart Disease ECG
Changes such as:
Q waves (indicating transmural infarcts)
ST-segment abnormalities
T-wave inversion
Arrhythmias

28. Ischemic Heart Disease Laboratory evaluation
Cardiac troponins T and I (TnT, TnI)
Creatine kinase (CK, and more specifically the myocardial-specific isoform, CK-MB)
Lactate dehydrogenase
Myoglobin
Troponins and CK-MB have high specificity and sensitivity for myocardial damage
macromolecules that leak out of injured myocardial cells through damaged cell membranes

29. Ischemic Heart Disease Laboratory evaluation
TnI and TnT are not normally detectable in the circulation
After acute MI both troponins:
Become detectable after 2 to 4 hours
Peak at 48 hours
Their levels remain elevated for 7 to 10 days

30. Ischemic Heart Disease Laboratory evaluation
CK-MB is the second best marker
CK-MB activity:
Begins to rise within 2 to 4 hours of MI
Peaks at 24 to 48 hours
Returns to normal within approximately 72 hours
, total CK activity is not a reliable marker of cardiac injury (i.e., it could come from skeletal muscle injury).
Although cardiac troponin and CK-MB are equally sensitive at early stages of an MI, persistence of elevated troponin levels for approximately 10 days allows the diagnosis of an acute MI long after CK-MB levels have returned to normal.

31. Ischemic Heart Disease Complications of MI
At least 80% will suffer:
Cardiogenic shock (>40% infarct of LV)
Congestive heart failureCHF
Arrhythmia
Rupture of ventricle, free wall, septum, or papillary muscle
Aneurysm formation,
Mural thrombus, potentially source of emboli
Pericarditis
Overall, however, patients with anterior infarcts have a substantially worse clinical course than those with posterior infarcts
Arrhythmia responsible for many deaths
Rupture will lead to cardiac tamponade, VSD, MR, most common 3-7 days post infarction (granulation tissue)
Thrombosis due to stasis and endocardial injury
Aneurysm lead to failure, thrombosis ,arrhythmia and no rupture

32. Ischemic Heart Disease MI death and complications rates
25% die, presumably due to arrythmia
10% of the rest will die within a month
80-90% will develop complications
Overall 30% die in the 1st year and then 10% per year
Number are not very consatant

36. Dressler’s

40. Chronic ischemic heart disease
Progressive heart failure due to ischemic injury, either from:
prior infarction(s) (most common)
chronic low-grade ischemia

41. Ischemic Heart Disease Sudden cardiac death
Unexpected death from cardiac causes either without symptoms or within 1 to 24 hours of symptom onset (different authors use different time points)
Results from a fatal arrhythmia, most commonly in patients with severe coronary artery disease

42. Ischemic Heart Disease Acute coronary syndrome
is applied to three catastrophic manifestations of IHD:
Unstable angina
Acute MI
Sudden cardiac death