HTN diabetes, palpitation with exertion at rest
SVT(supraventricular tachycardia) narrow complex tachycardia
cardiac enzyme(-)
how to determine stenosis %?
PCI? AP? ramus? LVH?
lateral wall moerately hypokinetic
atrial arrhythmia NOT RELATED TO ischemia
AVNRT, UVS
LD, femoral sheath?
ACC/AHA guideline
degree of aortic stenosis
class I, II, III
Gorlin formula
calculate valve area using cardiac output
calc systolic ejection period
Hakki 1981
Heart rate x SEP x 44.3 = 1
Hakki aortic valve area (AVA), normal aortic diameter (3.7 ~ 3.8 cm)
TR?
akinesis?
LVEDP? TTE?
antero apical akinesis vs. aneurysm?
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Medical tests that are often referred to as cardiac markers include:
- cardiac troponin (the most sensitive and specific test for myocardial damage)
- creatine kinase (CK, also known as phosphocreatine kinase or creatine phosphokinase)
- Aspartate transaminase (AST, also called Glutamic Oxaloacetic Transaminase (GOT/SGOT) or aspartate aminotransferase (ASAT))
- lactate dehydrogenase (LDH)
- Myoglobin (Mb) has low specificify for myocardial infarction and is used less than the other markers.
Cardiac markers are substances released from heart muscle when it is damaged as a result of myocardial infarction. Depending on the marker, it can take between 2 to 24 hours for the level to increase in the blood. Additionally, determining the levels of cardiac markers in the laboratory - like many other lab measurements - takes substantial time. Cardiac markers are therefore not useful in diagnosing a myocardial infarction in the acute phase. The clinical presentation and results from an ECG are more appropriate in the acute situation.
- Myocardial markers in myocardial infarction
Ischemia-Modified Albumin (IMA) can be detected via the albumin cobalt binding (ACB) test, a limited available FDA approved assay. Myocardial ischemia alters the N-terminus of albumin reducing the ability of cobalt to bind to albumin. IMA measures ischemia in the blood vessels and thus returns results in minutes rather than traditional markers of necrosis that take hours. ACB has low specificity therefore generating high number of false positives and must be used in conjunction with typical acute approaches such as ECG and physical exam. Additional studies are required.
--------------------------------------------------------------------------Troponin (tro-po'-nin) is a complex of proteins that is integral to muscle contraction. Troponin is attached to tropomyosin (another type of protein) and lies within the groove between actin (muscle) filaments. In a relaxed muscle, tropomyosin blocks the attachment of cross bridges to actin, thus preventing contraction. When the muscle cell is stimulated to contract, mechanisms cause the concentration of calcium in the sarcoplasm to rise. Some of this calcium attaches to troponin, causing a conformational change that moves troponin and tropomyosin out of the way so that the cross bridges can attach to actin and produce muscle contraction.
Troponin is found in both skeletal muscle and cardiac muscle, but the specific versions of troponin differ between types of muscle, due to the expression of different genes (in the heart, for example). The main difference is that the TnC subunit of troponin in skeletal muscle has 4 calcium ion binding sites, whereas in cardiac muscle there is only 3.
Discussions of troponin often pertain to its functional characteristics and/or to its usefulness as a diagnostic marker for various heart disorders.
Role of troponins
Both cardiac and skeletal muscles are exquisitely controlled by changes in the intracellular calcium concentration. When calcium rises, the muscles contract, and when calcium falls the muscles relax.
Troponin is a component of thin filaments (along with actin and tropomyosin), and is the protein to which calcium binds to accomplish this regulation. Troponin has three subunits, TnC, TnI, and TnT. When calcium is bound to specific sites on TnC, the structure of the thin filament changes in such a manner that myosin (a molecular motor organized in muscle thick filaments) attaches to thin filaments and produces force and/or movement. In the absence of calcium, tropomyosin interferes with this action of myosin, and therefore muscles remain relaxed.
Individual subunits serve different functions:
- Troponin C binds to calcium ions to produce movement
- Troponin T binds to tropomyosin, interlocking them to form a troponin-tropomyosin complex
- Troponin I binds to actin in thin myofilaments to hold the troponin-tropomyosin complex in place
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Creatine kinase (CK), also known as phosphocreatine kinase or creatine phosphokinase (CPK) is an enzyme (EC 2.7.3.2) expressed by various tissue types. Its function is the catalysis of the conversion of creatine to phosphocreatine, consuming adenosine triphosphate (ATP) and generating adenosine diphosphate (ADP) and the reverse reaction. In tissues that consume ATP rapidly, especially skeletal muscle, but also brain and smooth muscle, phosphocreatine serves as an energy reservoir for the rapid regeneration of ATP, the major source of energy in biochemical reactions.
Isoenzyme patterns differ in tissues. CK-BB occurs mainly in tissues, and its levels do rarely have any significance in bloodstream. Skeletal muscle expresses CK-MM (98%) and CK-MB at low levels (1%) in muscle. The myocardium (heart muscle), in contrast, expresses CK-MM at 70% and CK-MB at 30%.
Predominate Creatine Kinase Expresion
- MM - Skeletal Muscle
- MB - Cardiac Muscle
- BB - Brain Tissue
CK is often determined routinely in emergency patients. In addition, it is determined specifically in patients with chest pain and acute renal failure. Normal values are usually between 25 and 200 U/L. This test is not specific for the type of CK that is elevated.
Elevation of CK is an indication of damage to muscle. It is therefore indicative of injury, rhabdomyolysis, myocardial infarction, myositis, myocarditis, malignant hyperthermia and neuroleptic malignant syndrome. It is also seen in McLeod syndrome and hypothyroidism. The use of statin medications, which are commonly used to decrease serum cholesterol levels, may be associated with elevation of the CPK level in about 1% of the patients taking these medications, and with actual muscle damage in a much smaller proportion.
Lowered CK can be an indication of alcoholic liver disease and rheumatoid arthritis.
Isoenzyme determination has been used extensively as an indication for myocardial damage in heart attacks. Troponin measurement has largely replaced this in many hospitals, although some centres still rely on CK-MB.
--------------------------------------------------------------------------Aspartate Transaminase (AST) also called Serum Glutamic Oxaloacetic Transaminase (SGOT) or aspartate aminotransferase (ASAT) (EC 2.6.1.1) is similar to alanine transaminase (ALT) in that it is another enzyme associated with liver parenchymal cells. It is raised in acute liver damage. It is also present in red blood cells and cardiac muscle.
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Lactate dehydrogenase (LDH) is an enzyme (EC 1.1.1.27) present in a wide variety of organisms, including plants and animals. It catalyses the interconversion of pyruvate and lactate with concomitant interconversion of NADH and NAD+. As it can also catalyze the oxidation of hydroxybutyrate, it is occasionally called Hydroxybutyrate Dehydrogenase (HBD).
Enzyme isoforms
- LDH-1 (4H) - in the heart
- LDH-2 (3H1M) - in the reticuloendothelial system
- LDH-3 (2H2M) - in the lungs
- LDH-4 (1H3M) - in the kidneys
- LDH-5 (4M) - in the liver and striated muscle
Usually LDH-2 is the predominant form in the serum. An LDH-1 level higher than the LDH-2 level (a "flipped pattern"), suggests myocardial infarction (damage to heart tissues releases heart LDH, which is rich in LDH-1, into the bloodstream). The use of this phenomenon to diagnose infarction has been largely superseded by the use of Troponin I or T measurement.
Hemolysis
In medicine, LDH is often used as a marker of tissue breakdown. As LDH is abundant in red blood cells and can function as a marker for hemolysis. A blood sample that has been handled incorrectly can show false-positively high levels of LDH due to erythrocyte damage. It can also be used as a marker of myocardial infarction. Following a myocardial infarction, levels of LDH peak at 3-4 days and remain elevated for up to 10 days. In this way, elevated levels of LDH can be useful for determining if a patient has had a myocardial infarction if they come to doctors several days after an episode of chest pain.
[edit] Tissue turnover
Other uses are assessment of tissue breakdown in general; this is possible when there are no other indicators of hemolysis. It is used to follow-up cancer (especially lymphoma) patients, as cancer cells have a high rate of turnover, with destroyed cells leading to an elevated LDH activity.
[edit] Exudates and transudates
Measuring LDH in fluid aspirated from a pleural effusion (or pericardial effusion) can help in the distinction between exudates (actively secreted fluid, e.g. due to inflammation) or transudates (passively secreted fluid, due to a high hydrostatic pressure or a low oncotic pressure). LDH is elevated (>200 U/l) in an exudate and low in a transudate. In empyema, the LDH levels generally will exceed 1000 U/l.
[edit] Meningitis and encephalitis
The enzyme is also found in cerebrospinal fluid where high levels of lactate dehydrogenase in cerebrospinal fluid are often associated with bacterial meningitis. High levels of the enzyme can also be found in cases of viral meningitis, generally indicating the presence of encephalitis and poor prognosis.
[edit] HIV and elevated LDH
LDH is often measured in HIV patients as a non-specific marker for Pneumocystis jiroveci (formerly Pneumocystis carinii) pneumonia (PCP). Elevated LDH in the setting of upper respiratory symptoms in an HIV patient suggests, but is not diagnostic for, PCP.
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Myoglobin is a single-chain globular protein of 153 amino acids, containing a heme (iron-containing porphyrin) prosthetic group in the center around which the remaining apoprotein folds. With a molecular weight of 16,700 Daltons, it is the primary oxygen-carrying pigment of muscle tissues.[11] Unlike the blood-borne hemoglobin, to which it is structurally related,[12] this protein does not exhibit cooperative binding of oxygen, since positive cooperativity is a property reserved for multimeric proteins. Instead, the binding of oxygen by myoglobin is unaffected by the oxygen pressure in the surrounding tissue. Myoglobin is often cited as having an "instant binding tenacity" to oxygen given its hyperbolic oxygen dissociation curve.
Role in disease
Myoglobin is released from damaged muscle tissue (rhabdomyolysis), which has very high concentrations of myoglobin. The released myoglobin is filtered by the kidneys but is toxic to the renal tubular epithelium and so may cause acute renal failure.[15]
Myoglobin is a sensitive marker for muscle injury, making it a potential marker for heart attack in patients with chest pain.[16] Its lack of specificity and the cost of the analysis has prevented its widespread use.
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Markers in MI
Cardiac markers or cardiac enzymes are proteins from cardiac tissue found in the blood. These proteins are released into the bloodstream when damage to the heart occurs, as in the case of a myocardial infarction. Until the 1980s, the enzymes SGOT and LDH were used to assess cardiac injury. Then it was found that disproportional elevation of the MB subtype of the enzyme creatine kinase (CK) was very specific for myocardial injury. Current guidelines are generally in favor of troponin sub-units I or T, which are very specific for the heart muscle and are thought to rise before permanent injury develops.[58] Elevated troponins in the setting of chest pain may accurately predict a high likelihood of a myocardial infarction in the near future.[59]
The diagnosis of myocardial infarction requires two out of three components (history, ECG, and enzymes). When damage to the heart occurs, levels of cardiac markers rise over time, which is why blood tests for them are taken over a 24 hour period. Because these enzyme levels are not elevated immediately following a heart attack, patients presenting with chest pain are generally treated with the assumption that a myocardial infarction has occurred and then evaluated for a more precise diagnosis.[60]
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Percutaneous coronary intervention (PCI) is an invasive cardiologic therapeutic procedure to treat the stenotic (narrowed) coronary arteries of the heart.
Percutaneous coronary intervention can be performed to reduced or eliminate the symptoms of coronary artery disease, including angina (chest pain), dyspnea (shortness of breath) on exertion, and congestive heart failure. PCI is also used to abort an acute myocardial infarction, and in some specific cases it may reduce mortality.
During the procedure several options may be used:
- Balloon angioplasty
- Implantation of stents
- Rotational or laser atherectomy
- Brachytherapy
Brachy is from a Greek word for "short", so brachytherapy roughly translated is short distance therapy.
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AV nodal reentrant tachycardia (AVNRT) is a type of reentrant tachycardia (fast rhythm) of the heart. It is a supraventricular tachycardia, meaning that it originates from a location within the heart above the bundle of HIS.
In AVNRT, the fast pathway and the slow pathway are usually both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferiorly and slightly anterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node.
Common AVNRT
In common AVNRT, the anterograde conduction is via the slow pathway and the retrograde conduction is via the fast pathway ("slow-fast" AVNRT).
Because the retrograde conduction is via the fast pathway, stimulation of the atria (which produces the inverted P wave) will occur at the same time as stimulation of the ventricles (which causes the QRS complex). As a result, the inverted P waves may not be seen on the surface ECG since they are buried with the QRS complexes.
[edit] Uncommon AVNRT
In uncommon AVNRT, the anterograde conduction is via the fast pathway and the retrograde conduction is via the slow pathway ("fast-slow" AVNRT). Multiple slow pathways can exist so that both anterograde and retrograde conduction are over slow pathways. ("slow-slow" AVNRT).
Because the retrograde conduction is via the slow pathway, stimulation of the atria will be delayed by the slow conduction tissue and will typically produce an inverted P wave that falls after the QRS complex on the surface ECG.
[edit] Fast and slow pathways vs. accessory pathways
The fast and slow pathways should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW) syndrome or atrioventricular re-entrant tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium in close proximity to the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings, they provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
[edit] Treatment
An episode of supraventricular tachycardia (SVT) due to AVNRT can be terminated by any action that transiently blocks the AV node. This is because the AV node is an essential portion of the reentrant circuit in AVNRT.
Medical therapy can be initiated with AV nodal slowing drugs such as beta blockers or calcium channel blockers. Increasing vagul tone, such as coratid sinus massage, valsalva maneuver, or induced retching can help.
After being diagnosed with AVNRT, patients can also undergo an electrophysiology (EP) study to confirm the diagnosis and subsequent catheter ablation of the slow pathway which effectively cures the patient of AVNRT.
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Left ventricular hypertrophy (LVH) is the thickening of the myocardium (muscle) of the left ventricle of the heart. While ventricular hypertrophy can occur naturally as a reaction to aerobic exercise and strength training, it is most frequently referred to as a pathological reaction to cardiovascular disease.
While LVH itself is not a disease, it is usually a marker for disease involving the heart. Disease processes that can cause LVH include any disease that increases the afterload that the heart has to contract against, and some primary diseases of the muscle of the heart.
Causes of increased afterload that can cause LVH include aortic stenosis, aortic insufficiency, and hypertension. Primary disease of the muscle of the heart that cause LVH are known as hypertrophic cardiomyopathies.
--------------------------------------------------------------------------Hypertrophic cardiomyopathy, or HCM, is a disease of the myocardium (the muscle of the heart) in which a portion of the myocardium is hypertrophied (thickened) without any obvious cause [1] [2] [3] [4] [5] [6]. Though perhaps most famous as a leading cause of sudden cardiac death in young athletes [7] HCM's more important significance is as a cause of sudden unexpected cardiac death in any age group and as a cause of disabling cardiac symptoms.
A cardiomyopathy is any disease that primarily affects the muscle of the heart. In HCM, the normal alignment of muscle cells is disrupted, a phenomenon known as myocardial disarray. HCM also causes disruptions of the electrical functions of the heart. HCM is believed to be due to a mutation in one of many genes that results in a mutated myosin heavy chain, one of the components of the myocyte (the muscle cell of the heart). Depending on the degree of obstruction of the outflow of blood from the left ventricle of the heart, HCM can be defined as obstructive or non-obstructive.
Associated symptoms
The clinical course of HCM is variable. Many patients are asymptomatic or mildly symptomatic. The symptoms of HCM include shortness of breath, chest pain (sometimes known as angina), uncomfortable awareness of the heart beat (palpitations), lightheadedness, fatigue, fainting (called syncope) and sudden cardiac death. Dyspnea is largely due to increased stiffness of the left ventricle, which impairs filling of the ventricles and leads to elevated pressure in the left ventricle and left atrium. Symptoms are not closely related to the presence or severity of an outflow tract gradient [20].
Risk factors for sudden death in individuals with HCM include a young age at first diagnosis (age < href="http://en.wikipedia.org/wiki/Supraventricular_tachycardia" title="Supraventricular tachycardia">supraventricular or ventricular tachycardia, recurrent syncope, ventricular septal wall thickness over 3cm, hypotensive response to exercise, syncope (especially in children), and bradyarrhythmias (slow rhythms of the heart)[21]
[edit] Physical examination
| Aortic stenosis | Hypertrophic cardiomyopathy | |
|---|---|---|
| Echocardiography | ||
| Aortic valve calcification | Common | No |
| Dilated ascending aorta | Common | Rare |
| Ventricular hypertrophy | Concentric LVH | Asymmetric, often involving the septum |
| Physical examination | ||
| Murmur of AI | Common | No |
| Pulse pressure after PVC | Increased | Decreased |
| Valsalva maneuver | Decreased intensity of murmur | Increased intensity of murmur |
| Carotid pulsation | Normal or tardus et parvus | Brisk, jerky |
The physical findings of HCM are associated with the dynamic outflow obstruction that is often present with this disease.
Upon auscultation, the cardiac murmur will sound similar to the murmur of aortic stenosis. However, this murmur will increase in intensity with any maneuver that decreases the volume of blood in the left ventricle (such as standing or the strain phase of a Valsalva maneuver).
If dynamic outflow obstruction exists, physical examination findings that can be elicited include the pulsus bisferiens and the double apical impulse with each ventricular contraction. These findings, when present, can help differentiate HCM from aortic stenosis. In addition, if the individual has premature ventricular contractions (PVCs), the change in the carotid pulse intensity in the beat after the PVC can help differentiate HCM from aortic stenosis. In individuals with HCM, the pulse pressure will decrease in the beat after the PVC, while in aortic stenosis, the pulse pressure will increase.
--------------------------------------------------------------------------In medicine, pulsus tardus et parvus, is a sign where, on palpation of the pulse, the pulse is late (tardus) (relative to contraction of the heart) and weak/small (parvus). Classically, it seen in aortic valve stenosis.
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Gorlin formula
Flow across the AV = CO/SEP
|
| where ΔP = pressure gradient in mm Hg C = 1 for the AV and .85 for the MV. |
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Symptoms of aortic stenosis
When symptomatic, aortic stenosis can cause dizziness, syncope, angina and congestive heart failure. More symptoms indicate a worse prognosis. Treatment requires replacement of the diseased valve with either a prosthetic aortic valve.
[edit] Congestive heart failure
Congestive heart failure (CHF) is a grave prognosis in patients with AS. Patients with CHF that is attributed to AS have a 2 year mortality rate of 50%, if the aortic valve is not replaced.
CHF in the setting of AS is due to a combination of systolic dysfunction (a decrease in the ejection fraction) and diastolic dysfunction (elevated filling pressure of the LV).
[edit] Syncope
Syncope in the setting of heart failure increases the risk of death. In patients with syncope, the 3 year mortality rate is 50%, if the aortic valve is not replaced.
It is unclear why aortic stenosis causes syncope. One popular theory is that severe AS produces a nearly fixed cardiac output. When the patient exercises, their peripheral vascular resistance will decrease as the blood vesels of the skeletal muscles dilate to allow the muscles to receive more blood to allow them to do more work. This decrease in peripheral vascular resistance is normally compensated for by an increase in the cardiac output. Since patients with severe AS cannot increase their cardiac output, the blood pressure falls and the patient will syncopize due to decreased blood perfusion to the brain.
A second theory as to why syncope may occur in AS is that during exercise, the high pressures generated in the hypertrophied LV cause a vasodepressor response, which causes a secondary peripheral vasodilation which in turn causes decreased blood flow to the brain. Indeed, in aortic stenosis, because of the fixed obstruction to bloodflow out from the heart, it may be impossible for the heart to increase its output to offset peripheral vasodilation.
A third mechanism may sometimes be operative. Due to the hypertrophy of the left ventricle in aortic stenosis, including the consequent inability of the coronary arteries to adequately supply blood to the myocardium (see "Angina" below), arrhythmias may develop. These can lead to syncope.
Finally, in calcific aortic stenosis at least, the calcification in and around the aortic valve can progress and extend to involve the electrical conduction system of the heart. If that occurs, the result may be heart block - a potentially lethal condition of which syncope may be a symptom.
[edit] Angina
Angina in the setting of heart failure also increases the risk of death. In patients with angina, the 5 year mortality rate is 50%, if the aortic valve is not replaced.
Angina in the setting of AS is secondary to the left ventricular hypertrophy (LVH) that is caused by the constant production of increased pressure required to overcome the pressure gradient caused by the AS. While the myocardium of the LV gets thicker, the arteries that supply the muscle do not get significantly longer or bigger, so the muscle may become ischemic. The ischemia may first be evident during exercise, when the muscle requires increased blood supply to compensate for the increased workload. The individual may complain of exertional angina. At this stage, a stress test with imaging may be suggestive of ischemia.
Eventually, however, the muscle will require more blood supply at rest than can be supplied by the coronary artery branches. At this point there may be signs of ventricular strain pattern on the EKG, suggesting subendocardial ischemia. The subendocardium is the region that becomes ischemic because it is the most distant from the epicardial coronary arteries.
[edit] Associated symptoms
In Heyde's syndrome, aortic stenosis is associated with angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenosed valve.
