Archive for the ‘ L2-Patho IHD ’ Category

L2- Pathology of Ischemic Heart Disease

CLINICAL MANFESTATIOS OF ISCHEMIC HEART DISEASE

  • SIZE OF HE PROBLEM

  • ATHEROTHROMBOTIC CORONARY HEART DISEASE

  • RISK FACTORS FOR IHD

  • CLINICAL PRESENTATION

  • DIAGNOSIS AND INVESTIGATIONS

  • THERAPY

  • PREVENTION

SIZE OF THE PROBLEM

IHD is now the leading cause of death worldwide, and it is expected that the rate of IHD will accelerate in the next decades, contributed to by;

1.aging of population

2.Alarming increase in the prevalence of obesity, type 2 DM, and metabolic syndrome

3.Rise in CV risk factors (smoking, stress) among young generations

The WHO estimates that by 2020 the global number of deaths from IHD will have risen from 7.1 in 2002 to 11.1 millions

Picture1

FIGURE 35-2B The structure of normal arteries. A, Elastic artery. Note the concentric laminae of elastic tissue that form “sandwiches” with successive layers of smooth muscle cells. Each level of the elastic arterial tree has a characteristic number of elastic laminae. B, Muscular artery. The smooth muscle cells are surrounded by a collagenous matrix but lack the concentric rings of well organized elastic tissue characteristic of the larger arteries.

Picture2

FIGURE 35-3 The endothelial thrombotic balance. This diagram depicts the anticoagulant profibrinolytic functions of the endothelial cell  (left) and certain procoagulant and antifibrinolytic functions (right). PAi = plasminogen activator inhibitor; PGI2 = prostacyclin; t-PA = tissue type plasminogen activator; vWf = von Willebrand factor.

Picture3

FIGURE 35-4 Schematic of the evolution of the atherosclerotic plaque. 1: Accumulation of lipoprotein particles in the intima. The modification of these lipoproteins is depicted by the darker color. Modifications include oxidation and glycation. 2: Oxidative stress, including products found in modified lipoproteins, can induce local cytokine elaboration. 3: The cytokines thus induced increase expression of adhesion molecules for leukocytes that cause their attachment and chemoattractant molecules that direct their migration into the intima. 4: Blood monocytes, upon entering the artery wall in response to chemoattractant cytokines such as monocyte chemoattractant protein 1 (MCP-1), encounter stimuli such as macrophage colony stimulating factor (M-CSF) that can augment their expression of scavenger receptors. 5: Scavenger receptors mediate the uptake of modified lipoprotein particles and promote the development of foam cells. Macrophage foam cells are a source of mediators such as further cytokines and effector molecules such as hypochlorous acid, superoxide anion (O2-), and matrix metalloproteinases. 6: Smooth muscle cells in the intima divide other smooth muscle cells that migrate into the intima from the media. 7: Smooth muscle cells can then divide and elaborate extracellular matrix, promoting extracellular matrix accumulation in the growing atherosclerotic plaque. In this manner, the fatty streak can evolve into a fibrofatty lesion. 8: In later stages, calcification can occur (not depicted) and fibrosis continues, sometimes accompanied by smooth muscle cell death (including programmed cell death, or apoptosis) yielding a relatively acellular fibrous capsule surrounding a lipid-rich core that may also contain dying or dead cells and their detritus. IL-1 = interleukin-1; LDL = low-density lipoprotein.

Picture4

FIGURE 35-5 Scanning electron micrograph of a freeze etch preparation of rabbit aorta following an intravenous injection of human low-density lipoprotein (LDL). Round LDL particles decorate the strands of proteoglycan found in the subendothelial region of the intima. By binding LDL particles, proteoglycan molecules can retard their traversal of the intima and promote their accumulation. Proteoglycan-associated LDL appears particularly susceptible to oxidative modification. Accumulation of extracellular lipoprotein particles is one of the first morphological changes noted after initiation of an atherogenic diet in experimental animals. (From Nievelstein PF, Fogelman AM, Mottino G, Frank JS: Lipid accumulation in rabbit aortic intima 2 hours after bolus infusion of low density lipoprotein: A deep-etch and immunolocalization study of ultrarapidly frozen tissue. Arterioscler Thromb 11:1795, 1991.)

Picture5

FIGURE 35-6C Electron microscopic examination of leukocyte interactions with the artery wall in hypercholesterolemic nonhuman primates. A and B, Scanning electron micrographs that demonstrate the adhesion of mononuclear phagocytes to the intact endothelium 12 days after initiating a hypercholesterolemic diet. C and D, Transmission electron micrographs. Note the abundant interdigitations and intimate association of the monocyte with the endothelium in part C. In part D, a monocyte appears to diapedese between two endothelial cells to enter the intima. (From Faggiotto A, Ross R, Harker L: Studies of hypercholesterolemia in the nonhuman primate. I. Changes that lead to fatty streak formation. Arteriosclerosis 4:323, 1984.)

Picture6

FIGURE 35-10 An example of a ruptured plaque that caused a fatal thrombosis. A, Movat stain. B, Immunostaining with HHF-35 discloses smooth muscle cells. Note the paucity of smooth muscle cells in the fibrous cap (white arrowheads), in contrast with the abundant smooth muscle cells in the medial layer (inset, M denotes the tunica media). C, Macrophage staining (CD-68) shows accumulation of the inflammatory cells near the fibrous cap (inset, F denotes foam cell). EEL = external elastic lamina; IEL = internal elastic lamina. (From Bezerra HG, Higuchi ML, Gutierrez PS, et al: Atheromas that cause fatal thrombosis are usually large and frequently accompanied by vessel enlargement. Cardiovasc Pathol 10:189, 2001.)

Picture7

FIGURE 35-11A Superficial erosion of experimental atherosclerotic lesions shown by scanning electron microscopy. Advanced atherosclerotic plaques can promote thrombosis by superficial erosion of the endothelial layer, exposing the blood and platelets to the subendothelial basement membrane containing collagen platelet activation and thrombosis. A, In the low-power view, the rent in the endothelium is evident. Leukocytes have adhered to the subendothelium, which is beginning to be covered with a carpet of platelets (arrows). B, The high-power view shows a field selected from the center of part A that shows the leukocytes and platelets adherent to the subendothelium. C, A low-power histological section through a coronary artery thrombosed due to superficial erosion. D, A higher power histological section through a coronary artery thrombosed due to superficial erosion. L = lumen; T = thrombus. (A & B, from Faggiotto A, Ross R: Studies of hypercholesterolemia in the nonhuman primate. II. Fatty streak conversion to fibrous plaque. Arteriosclerosis 4: 341, 1984. C & D, from Farb A, Burke AP, Tang AL, et al: Coronary plaque erosion without rupture into a lipid core: A frequent cause of coronary thrombosis in sudden coronary death. Circulation 93:1354, 1996.)

Picture8

FIGURE 35-11C Superficial erosion of experimental atherosclerotic lesions shown by scanning electron microscopy. Advanced atherosclerotic plaques can promote thrombosis by superficial erosion of the endothelial layer, exposing the blood and platelets to the subendothelial basement membrane containing collagen platelet activation and thrombosis. A, In the low-power view, the rent in the endothelium is evident. Leukocytes have adhered to the subendothelium, which is beginning to be covered with a carpet of platelets (arrows). B, The high-power view shows a field selected from the center of part A that shows the leukocytes and platelets adherent to the subendothelium. C, A low-power histological section through a coronary artery thrombosed due to superficial erosion. D, A higher power histological section through a coronary artery thrombosed due to superficial erosion. L = lumen; T = thrombus. (A & B, from Faggiotto A, Ross R: Studies of hypercholesterolemia in the nonhuman primate. II. Fatty streak conversion to fibrous plaque. Arteriosclerosis 4: 341, 1984. C & D, from Farb A, Burke AP, Tang AL, et al: Coronary plaque erosion without rupture into a lipid core: A frequent cause of coronary thrombosis in sudden coronary death. Circulation 93:1354, 1996.)

RISK FACTORS FOR IHD

NON MODIFIABLE

1.sex

2.age

3.family history

MODIFIABLE

1.Smoking

2.Stress

3.Hyperlipidemia

4. Obesity

5.Diabetes mellitus

6.Hypertension

7.others

Clinical presentation

  1. Silent
  2. Stable angina pectoris
  3. Acute coronary syndrome ( STEMI, UA AND NSTEMI)
  4. Heart failure
  5. Cardiac arrythmia
  6. Sudden cardiac death

DIAGNOSIS

  1. CLINICAL EVALUATION
  2. ECG: resting, stress
  3. LABORATORY TESTS
  4. ECHODOPPLER
  5. MYOCARDIAL PERFUSION SCAN
  6. CARDIAC CATHERIZATION AND CORONARY ANGIOGRAPHY

Picture9

TABLE 46-4 Molecular Biomarkers for the Evaluation of Patients with ST-Elevation Myocardial Infarction

THERAPY

Medical

Interventional;

-percutaneous coronary angioplasty and stentiong (PTCA)

Surgical ;

-coronary artery bypass grafing (CABG)

PREVENTION

PRIMARY

SECONDARY

Picture10

FIGURE 52-6 Key components of the Guardwire Distal Protection Balloon. The Guardwire device is advanced through the saphenous vein graft (SVG) to a distal portion of the SVG that is free of significant stenosis. The occlusion balloon is inflated and, after demonstration of occlusion, stent placement is performed within the SVG. At the end of stent deployment, an Export catheter is advanced and approximately 40 ml of blood and particulate material are removed. (From Baim D, Wahr D, George B, et al: Randomized trial of a distal embolic protection device during percutaneous intervention of saphenous vein aorto-coronary bypass grafts. Circulation 105:1285, 2002. Reproduced with permission.)

Picture11

FIGURE 52-2A A, Sequential restenoses within a long stent within the right coronary artery. B, A 3.5-mm × 15-mm cutting balloon is advanced across the in-stent restenosis and inflated. C, The cutting balloon is positioned more proximally and a repeated inflation is performed. D, At the end of the cutting balloon inflation, there is a 10 percent residual stenosis. The cutting balloon limits slippage of the balloon within the stent because of the longitudinal cutting blades that score the plaque while inflating the balloon.

Picture12

FIGURE 52-2B A, Sequential restenoses within a long stent within the right coronary artery. B, A 3.5-mm × 15-mm cutting balloon is advanced across the in-stent restenosis and inflated. C, The cutting balloon is positioned more proximally and a repeated inflation is performed. D, At the end of the cutting balloon inflation, there is a 10 percent residual stenosis. The cutting balloon limits slippage of the balloon within the stent because of the longitudinal cutting blades that score the plaque while inflating the balloon.

Picture13

FIGURE 52-2C A, Sequential restenoses within a long stent within the right coronary artery. B, A 3.5-mm × 15-mm cutting balloon is advanced across the in-stent restenosis and inflated. C, The cutting balloon is positioned more proximally and a repeated inflation is performed. D, At the end of the cutting balloon inflation, there is a 10 percent residual stenosis. The cutting balloon limits slippage of the balloon within the stent because of the longitudinal cutting blades that score the plaque while inflating the balloon.

Picture14

FIGURE 52-2D A, Sequential restenoses within a long stent within the right coronary artery. B, A 3.5-mm × 15-mm cutting balloon is advanced across the in-stent restenosis and inflated. C, The cutting balloon is positioned more proximally and a repeated inflation is performed. D, At the end of the cutting balloon inflation, there is a 10 percent residual stenosis. The cutting balloon limits slippage of the balloon within the stent because of the longitudinal cutting blades that score the plaque while inflating the balloon.

Case 5

The faint heart

GP visit

PERSONAL DATA:

Mrs. khan, 53 years old, obse

FAMILY  HISTORY:

her father died from heart attack in his fifties

SYMPTOMS:

chest pain, retrosternal, referred to lower jaw and back, precipitated by exercise especially in cold weather, relieved by rest.

PHYSICAL SIGNS

1.obese

2.Bp : 148/94 mmHg

INVESTIGATIONS

1.RESTING 12-LEAD ECG: normal

2.Blood glucose: normal

3.Serum lipids : hyperlipidemia with decreased HDL

TREATMENT

1.Healthy lifstyle

2.Drugs : aspirin, atenolol and GTN

Picture15

FIGURE 9-4 Top, Electrode connections for recording the three bipolar limb leads I, II, and III. R, L, and F indicate locations of electrodes on the right arm, the left arm, and the left foot, respectively. Bottom, Electrode locations and electrical connections for recording a unipolar precordial lead. Left, The positions of the exploring electrode (V) for the six precordial leads. Right, Connections to form the Wilson central terminal for recording a precordial (V) lead. (From Goldberger AL: Clinical Electrocardiography: A Simplified Approach. 6th ed. St Louis, CV Mosby, 1999.)

Picture16

FIGURE 9-11 The waves and intervals of a normal electrocardiogram. (From Goldberger AL: Clinical Electrocardiography: A Simplified Approach. 6th ed. St Louis, CV Mosby, 1999.)

Picture17

FIGURE 9-12 Normal electrocardiogram recorded from a 48-year-old woman. The vertical lines of the grid represent time, with lines spaced at 40 msec intervals. Horizontal lines represent voltage amplitude, with lines spaced at 0.1 mV intervals. Every fifth line in each direction is typically darkened. The heart rate is approximately 72 beats/min; the PR interval, QRS, and QTc durations measure about 140, 84, and 400 msec, respectively; and the mean QRS axis is approximately +35 degrees.

Medical emergency

Symptoms:

Sudden severe chest pain, prolonged, more than 1 hour

Physical signs

1.Mrs. Khan  was pale, clammy and in agony

2.BP: 100/60

3.Pulse: 60/min

Picture18

FIGURE 9-36B Current-of-injury patterns with acute ischemia. With predominant subendocardial ischemia (A), the resultant ST vector is directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore record ST depression. With ischemia involving the outer ventricular layer (B) (transmural or epicardial injury), the ST vector is directed outward. Overlying leads record ST elevation. Reciprocal ST depression can appear in contralateral leads.

Picture19

FIGURE 9-37 Hyperacute phase of extensive anterior-lateral myocardial infarction. Marked ST elevation melding with prominent T waves is present across the precordium, as well as in leads I and aVl. ST depression, consistent with a reciprocal change, is seen in leads III and aVf. Q waves are present in leads V3 through V6. Marked ST elevations with tall T waves caused by severe ischemia are sometimes referred to as a monophasic current-of-injury pattern. A paradoxical increase in R wave amplitude (V2 and V3) may accompany this pattern. This tracing also shows left axis deviation with small or absent inferior R waves, which raises the possibility of a prior inferior infarct.

Picture20

FIGURE 9-38A Sequence of depolarization and repolarization changes with (A) acute anterior-lateral and (B) acute inferior wall Q wave infarctions. With anterior-lateral infarcts, ST elevation in leads I, aVl, and the precordial leads can be accompanied by reciprocal ST depression in leads II, III, and aVf. Conversely, acute inferior (or posterior) infarcts can be associated with reciprocal ST depression in leads V1 to V3. (Modified from Goldberger AL: Clinical Electrocardiography: A Simplified Approach. 6th ed. St Louis, CV Mosby, 1999.)

Picture21

FIGURE 9-38B Sequence of depolarization and repolarization changes with (A) acute anterior-lateral and (B) acute inferior wall Q wave infarctions. With anterior-lateral infarcts, ST elevation in leads I, aVl, and the precordial leads can be accompanied by reciprocal ST depression in leads II, III, and aVf. Conversely, acute inferior (or posterior) infarcts can be associated with reciprocal ST depression in leads V1 to V3. (Modified from Goldberger AL: Clinical Electrocardiography: A Simplified Approach. 6th ed. St Louis, CV Mosby, 1999.)

INVETIGATIONS

ECG : anterior wall myocardial infarction

Biochemical test: elevated cardiac troponin T level

Cardiac catheterization and coronary angiography:

  1. Atherothrombotic lesions in the coronaries (diagnostic procedure)
  2. Balloon dilatation and stenting (percutaneous cornoary angioplasty)

TREATMENT

MEDICAL

  1. Oxygen
  2. Antiplatlets: aspirin and clopidogrel
  3. Analgesics and pain killers: diamorphine
  4. fibrinolytic: recombinant tissue plasminogen activator (rtpa)
  5. Angitensin converting enzyme inhibitor:Ramipril
  6. Beta blocker: atenolol
  7. Vasodilator:Glyceryl trinitrate
  8. Hypolipidemic : atrovastatin

INTERVENTIONAL (catheter-based)

1.Balloon dilatation and stenting (percutaneous cornoary angioplasty; PTCA)

PREVENTION

1.PRIMARY PERVENTION

2.SECONDARY PREVENTION AND REHABITILATION

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