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.
HCM is also known as idiopathic hypertrophic subaortic stenosis (IHSS) and
hypertrophic obstructive cardiomyopathy (HOCM). A non-obstructive variant of HCM is apical hypertrophic
cardiomyopathy [8], which is also known as nonobstructive hypertrophic cardiomyopathy
and Japanese variant hypertrophic cardiomyopathy (since the first cases described were all in individuals of
Japanese descent).
While most literature so far focuses on European, American, and Japanese populations, HCM appears in all racial groups. The
incidence of HCM is about 0.2% to 0.5% of the general population.
Genetics
Hypertrophic cardiomyopathy is inherited as an autosomal dominant trait and is
attributed to mutations in one of a number of genes that encode for one of the sarcomere
proteins including beta-cardiac myosin heavy chain (the first gene identified), cardiac actin,
cardiac troponin T, alpha-tropomyosin, cardiac troponin I, cardiac myosin-binding protein C, and the myosin light chains.
Currently there are more than 400 mutations in these genes. Approximately 45% of these mutations occur in the β myosin heavy chain gene on chromosome 14 q11.2-3) while approximately 35%
involve the cardiac myosin binding protein C gene. The prognosis is variable, based on the gene mutation. In individuals without
a family history of HCM, the most common cause of the disease is a de novo mutation of the gene
that produces the β-myosin heavy chain.
An insertion/deletion polymorphism in the gene encoding for angiotensin converting enzyme (ACE) alters the clinical phenotype of the disease. The D/D (deletion/deletion) genotype of ACE is associated with more marked
hypertrophy of the left ventricle and may be associated with higher risk of adverse outcomes [9] [10].
Anatomic characteristics
Individuals with HCM have some degree of left ventricular hypertrophy.
Usually this is an asymmetric hypertrophy, involving the inter-ventricular septum, and is known as asymmetric septal hypertrophy (ASH). This is in contrast to the concentric hypertrophy seen in aortic stenosis or hypertension. About two-thirds of
individuals with HCM have asymmetric septal hypertrophy.
About 25% of individuals with HCM demonstrate an obstruction to the outflow of blood from the left ventricle during rest. In
other individuals obstruction only occurs under certain conditions. This is known as dynamic outflow obstruction, because the
degree of obstruction is variable and is dependent on the amount of blood in the ventricle immediately before ventricle
systole (contraction).
Dynamic outflow obstruction
Dynamic outflow obstruction (when present in HCM) is usually due to systolic anterior motion
(SAM) of the anterior leaflet of the mitral valve. Systolic anterior motion of the mitral
valve (SAM) was initially thought to be due to the septal subaortic bulge, narrowing the outflow tract, causing high velocity
flow and a Venturi effect — a local underpressure in the outflow tract. Low pressure was
thought to suck the mitral valve anteriorly into the septum. But SAM onset is observed to be a low velocity phenomenon: SAM
begins at velocities no different from those measured in normals [11] [12]. Hence, the magnitude and importance of
Venturi forces in the outflow tract are much less than previously thought, and Venturi forces cannot be the main force that
initiates SAM.
Recent echocardiographic evidence indicates that drag, the pushing force of flow is the dominant hydrodynamic force on the
mitral leaflets [11] [12] [13] [14] [15] [16]. In obstructive HCM the mitral leaflets are often
large [17] and are anteriorly positioned in the LV cavity [11] [18] due to
anteriorly positioned papillary muscles[11] that at surgery are often "agglutinated" onto the LV anterior wall by
abnormal attachments [15] [16].
The mid-septal bulge aggravates the malposition of the valve and redirects outflow so that it comes from a lateral and
posterior direction[13]. The abnormally directed outflow may be visualized behind and lateral to the
enlarged mitral valve, where it catches it, and pushes it into the septum [11] [12] [13] [14]. There is a crucial overlap between the inflow
and outflow portions of the left ventricle [19]. As SAM progresses in early systole the angle between outflow and the
protruding mitral leaflet increases. A greater surface area of the leaflets is now exposed to drag which amplifies the force on
the leaflets – drag increases with increasing angle relative to flow[13]. An analogy is an open door in a drafty corridor: the
door starts by moving slowly and then accelerates as it presents a greater surface area to the wind and finally it slams shut.
The necessary conditions that predispose to SAM are: anterior position of the mitral valve in the LV, altered LV geometry that
allows flow to strike the mitral valve from behind, and chordal slack [11] [12] [13] [14]. SAM may considered anteriorly directed mitral
prolapse [12] [13] [14]. In both conditions the mitral valve is enlarged and
is displaced in systole by the pushing force of flow resulting in mitral regurgitation.
Because the mitral valve leaflet doesn't get pulled into the LVOT until after the aortic valve opens, the initial upstroke of
the arterial pulse will be normal. When the mitral valve leaflet gets pushed into the LVOT, the arterial pulse will momentarily
collapse and be followed by a second rise, as the left ventricular pressure overcomes the increased obstruction that SAM of the
mitral valve causes. This can be seen on the physical examination as a double tap upon palpation of the apical impulse and as a
double pulsation upon palpation of the carotid pulse, known as pulsus
bisferiens.
Associated symptoms
The clinical course of HCM is variable. Many patients are asymptomatic or mildly symptomatic. The symptoms of HCM include dyspnea (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]. Oftentimes, symptoms mimic
those of congestive heart failure (esp. activity intolerance & dyspnea), but it must
be noted that treatment is very different. To treat with diuretics (a mainstay of CHF treatment) will exacerbate symptoms in
hypertrophic cardiomyopathy by decreasing ventricular volume and increasing outflow resistance.
Risk factors for sudden death in individuals with HCM include a young age at first diagnosis (age < 30 years), an episode
of aborted sudden death, a family history of HCM with sudden death of relatives, specific mutations in the genes encoding for
troponin T and myosin, sustained 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]
Physical examination
Differentiating hypertrophic cardiomyopathy and valvular aortic stenosis
| |
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, or bisferiens pulse (a collapse of the pulse followed by a secondary rise) |
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.
Diagnostic testing
A diagnosis of hypertrophic cardiomyopathy is based upon a number of features of the
disease process. While there is use of echocardiography, cardiac catheterization, or cardiac MRI in
the diagnosis of the disease, other important factors include ECG findings and if
there is any family history of HCM or unexplained sudden death in otherwise healthy individuals.
Cardiac catheterization
Pressure tracings demonstrating the Brockenbrough–Braunwald–Morrow sign
AO = Descending aorta; LV = Left ventricle; ECG = Electrocardiogram.
After the third QRS complex, the ventricle has more time to fill. Since there is more
time to fill, the left ventricle will have more volume at the end of diastole (increased
preload). Due to the Frank–Starling law of the heart, the contraction of the left ventricle (and pressure
generated by the left ventricle) will be greater on the subsequent beat (beat #4 in this picture). Because of the dynamic nature
of the outflow obstruction in HCM, the obstruction increases more that the left ventricular pressure increase. This causes
a fall in the aortic pressure as the left ventricular pressure rises (seen as the yellow shaded area in the
picture).
Upon cardiac catheterization, catheters can
be placed in the left ventricle and the ascending aorta, to measure the pressure difference
between these structures. In normal individuals, during ventricular systole, the
pressure in the ascending aorta and the left ventricle will equalize, and the aortic valve is open. In individuals with
aortic stenosis or with HCM with an outflow tract gradient, there will be a
pressure gradient (difference) between the left ventricle and the aorta, with the left ventricular pressure higher than the
aortic pressure. This gradient represents the degree of obstruction that has to be overcome in order to eject blood from the left
ventricle.
The Brockenbrough–Braunwald–Morrow sign is observed in individuals with HCM with outflow tract gradient. This sign can
be used to differentiate HCM from aortic stenosis. In individuals with aortic stenosis, after a premature ventricular contraction (PVC), the following ventricular contraction will be
more forceful, and the pressure generated in the left ventricle will be higher. Because of the fixed obstruction that the
stenotic aortic valve represents, the post-PVC ascending aortic pressure will increase as well. In individuals with HCM, however,
the degree of obstruction will increase more than the force of contraction will increase in the post-PVC beat. The result of this
is that the left ventricular pressure increases and the ascending aortic pressure decreases, with an increase in the LVOT
gradient.
While the Brockenbrough–Braunwald–Morrow sign is most dramatically demonstrated using simultaneous intra-cardiac and
intra-aortic catheters, it can be seen on routine physical examination as a decrease in the pulse pressure in the post-PVC beat
in individuals with HCM.
Treatment
In all patients with hypertrophic cardiomyopathy risk stratification is essential to attempt to ascertain which patients are
at risk for sudden cardiac death [2]
[5]. In those patients deemed to be at high risk the benefits and infrequent
complications of defibrillator therapy are discussed; devices have been implanted in as many as 15% of patients at HCM centers.
Treatment symptoms of obstructive HCM is directed towards decreasing the left ventricular outflow tract gradient and symptoms of
dyspnea, chest pain and syncope. Medical therapy is successful in the majority of patients. The first medication that is
routinely used is beta-blockade (metoprolol, atenolol,
bisoprolol, propranolol)[2]. If symptoms and gradient persist disopyramide may be added to the
beta-blocker [22]. Alternately a calcium channel blocker such as verapamil may be substituted for beta-blockade. It should be stressed that most patient's symptoms may be
managed medically without needing to resort to inteventions such as surgical septal myectomy, alcohol septal ablation or pacing.
Severe symptoms in non-obstructive HCM may actually be more difficult to treat because there is no obvious target (obstruction)
to treat. Medical therapy with verapamil, beta-blockade may improve symptoms. Diuretics should
be avoided, as they reduce the intravascular volume of blood, decreasing the amount of blood available to distend the left
ventricular outflow tract, leading to an increase in the obstruction to the outflow of blood in the left ventricle [23].
Surgical myectomy
Surgical septal myectomy is the gold standard for relief of symptoms for patients who
do not experience relief of symptoms from medications [2] [3] [5] [6] [22] [24]. It has been performed successfully for more than 25 years. Surgical septal myectomy
uniformly decreases left ventricular outflow tract obstruction and improves symptoms, and in experienced centers has a surgical
mortality of 1%. It involves a midline thoracotomy (general anesthesia, opening the chest, and cardiopulmonary bypass) and
removing a portion of the interventricular septum[2]. Surgical myectomy resection focused just on the subaortic septum, to increase the size of
the outflow tract to reduce Venturi forces may be inadequate to abolish systolic anterior motion (SAM) of the anterior leaflet of
the mitral valve. With this limited sort of resection the residual mid-septal bulge still redirects flow posteriorly: SAM
persists because flow still gets behind the mitral valve. It is only when the deeper portion of the septal bulge is resected that
flow is redirected anteriorly away from the mitral valve, abolishing SAM [3] [25]. With this in mind, a modification of the Morrow myectomy termed
extended myectomy, mobilization and partial excision of the papillary muscles has become the excision of choice [3] [15] [16]
[26]. In selected patients with particularly large redundant mitral valves,
anterior leaflet plication may be added to complete separation of the mitral valve and outflow [26]
[27].
Alcohol septal ablation
Alcohol septal ablation, introduced by Ulrich Sigwart in 1994, is a percutaneous technique that involves injection of alcohol
into the first septal perferator of the left anterior descending artery. This is a
technique with results similar to the surgical septal myectomy procedure but is less invasive, since it does not involve general
anaesthesia and opening of the chest wall and pericardium (which are done in a septal myomectomy). In a select population with
symptoms secondary to a high outflow tract gradient, alcohol septal ablation can reduce the symptoms of HCM.[2][5][28]
When performed properly, an alcohol septal ablation induces a controlled heart
attack, in which the portion of the interventricular septum that involves the left ventricular outflow tract is infarcted
and will contract into a scar.
Ventricular pacing
The use of a pacemaker has been advocated in a subset of individuals, in order
to cause asynchronous contraction of the left ventricle. Since the pacemaker activates the interventricular septum before the
left ventricular free wall, the gradient across the left ventricular outflow tract may decrease. This form of treatment has been
shown to provide less relief of symptoms and less of a reduction in the left ventricular outflow tract gradient when compared to
surgical myectomy [29].
Cardiac transplantation
In cases that are refractory to all other forms of treatment, cardiac
transplantation is an option.
Related disorders
Feline hypertrophic cardiomyopathy is the most common heart disease in
cats; the disease process and genetics are believed to be similar to the disease in humans.[30] The first genetic mutation (in cardiac myosin binding protein C)
responsible for feline hypertrophic cardiomyopathy was discovered in 2005 in Maine Coon
cats.[31] A test for this mutation is available.[32] About one third of Maine Coon cats tested for the mutation have been shown to be
either heterozygous and homozygous for the mutation, although many of these cats have no clinical signs of the disease. Some
Maine Coon cats with clinical evidence of hypertrophic cardiomyopathy test negative for this mutation, strongly suggesting that a
second mutation exists in the breed. The cardiac myosin binding protein C mutation has not been found in any other breed of cat
with HCM.
HCM in popular culture
In the CW television show One Tree Hill, characters Dan and Lucas Scott have HCM.
Vivian Johnson on Without a Trace also has HCM.
On the TV series Scrubs, in the first episode involving Jordan, Dr Kelso
tells JD to run tests to check her for HCM.
One of the players in Glory Road was benched with HCM.
References
- ^ Richardson
P, McKenna W, Bristow M, Maisch B, Mautner B, O'Connell J, Olsen E, Thiene G, Goodwin J, Gyarfas I, Martin I, Nordet P. Report of
the 1995 World Health Organization/International Society and Federation of Cardiology Task Force on the Definition and
Classification of cardiomyopathies. Circulation. 1996 Mar 1;
93(5):841–2. (Medline abstract; Full text)
- ^ a b c d e f Maron B. Hypertrophic cardiomyopathy: a systematic review.
JAMA 2002. 287:1308–20
- ^ a
b c d Sherrid M, Chaudhry FA, Swistel DG. Obstructive
hypertrophic cardiomyopathy. Echocardiography, pathophysiology, and the continuing evolution of surgery for obstruction.
Annals of Thoracic Surgery 2003; 75:620–32
- ^ Wigle D, Sasson Z,
Henderson MA, Ruddy TD, Fulop J, Rakowski H, Williams WG. Hypertrophic cardiomyopathy. The importance of the site and the extent
of hypertrophy. A review. Progress in Cardiovascular Diseases 1985; 28:1–83
- ^ a
b c d Wigle ED, Rakowski H, Kimball BP, Williams WG.
Hypertrophic cardiomyopathy — clinical spectrum and treatment. Circulation
1995; 92:1680–92
- ^ a
b Maron BJ, McKenna WJ, Danielson GK, Kappenberger
LJ, Kuhn HJ, Seidman CE, Shah PM, Spencer WH III, Spirito P, Ten Cate FJ, Wigle ED. American College of Cardiology / European Society of Cardiology clinical expert consensus document on hypertrophic
cardiomyopathy. J Am Coll Cardiol. 2003; 42:1687–713
- ^ Maron BJ, Thompson
PD, Puffer JC, McGrew CA, Strong WB, Douglas PS, Clark LT, Mitten MJ, Crawford MH, Atkins DL, Driscoll DJ, Epstein AE.
Cardiovascular preparticipation screening of competitive athletes. A statement for health professionals from the Sudden Death
Committee (clinical cardiology) and Congenital Cardiac Defects Committee (cardiovascular disease in the young), American Heart
Association. Circulation. 1996 Aug 15; 94(4):850-6. (Medline abstract; Full text)
- ^ Rivera-Diaz J, Moosvi
AR. Apical hypertrophic cardiomyopathy. South Med J. 1996 Jul; 89(7):711-3.
(Medline abstract; Full text)
- ^ Doolan G, Nguyen L,
Chung J, Ingles J, Semsarian C. Progression of left ventricular hypertrophy and the angiotensin-converting enzyme gene
polymorphism in hypertrophic cardiomyopathy. Int J Cardiol. 2004 Aug; 96(2):157–63.
(Medline abstract)
- ^ Marian AJ, Yu QT, Workman R,
Greve G, Roberts R. Angiotensin-converting enzyme polymorphism in hypertrophic cardiomyopathy and sudden cardiac death.
Lancet. 1993 Oct 30; 342(8879):1085–6. (Medline abstract)
- ^ a
b c d e f Jiang L, Levine RA, King ME, Weyman AE. An integrated
mechanism for systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy based on echocardiographic
observations. Am Heart J 1987; 113:633–44
- ^ a b c d e Sherrid MV, Gunsburg DZ, Moldenhauer S, Pearle G.
Systolic anterior motion begins at low left ventricular outflow tract velocity in obstructive hypertrophic cardiomyopathy.
J Am Coll Cardiol 2000; 36:1344–54
- ^ a
b c d e f Sherrid MV, Chu Ck, DeLia E, Mogtader A, Dwyer Jr. EM, An
echocardiographic study of the fluid mechanics of obstruction in hypertrophic cardiomyopathy. J Am
Coll Cardiol 1993; 22:816–25
- ^ a b c d Levine RA, Vlahakes GJ, Lefebvre X, et al. Papillary
muscle displacement causes systolic anterior motion of the mitral valve. Circulation 1995; 91:1189–95
- ^ a b c Messmer
BJ. Extended myectomy for hypertrophic obstructive cardiomyopathy. Ann Thorac Surg 1994;
58:575–7
- ^ a b c Schoendube FA, Klues HG, Reith S, Flachskampf FA,
Hanrath P, Messmer BJ. Long-term clinical and echocardiographic follow-up after surgical correction of hypertrophic obstructive
cardiomyopathy with extended myectomy and reconstruction of the subvalvular mitral apparatus. Circulation 1995; 92:II-122–7
- ^ Klues HG, Maron BJ,
Dollar AL, Roberts WC. Diverstiy of structural mitral valve alterations in hypertrophic cardiomyopathy. Circulation 1992; 85:1651–60
- ^ Henry WL, Clark CE,
Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal
hypertrophy (idiopathic hypertrophic subaortic stenosis). Am J Cardiol 1975;
35:337–45
- ^ Schwammenthal E,
Levine RA. Dynamic subaortic obstruction: a disease of the mitral valve suitable for surgical repair? J Am Coll Cardiol 1996; 28:203–6
- ^ Braunwauld E. The Cardiomyopathies, in
Braunwald's Heart Disease, 7th ed, D Zipes, et al (eds). Philadelphia, Saunders, 2005
- ^ Maron BJ, Cecchi F,
McKenna WJ. Risk factors and stratification for sudden cardiac death in patients with hypertrophic cardiomyopathy.
Br Heart J. 1994 Dec; 72(6 Suppl):S13–8. (Medline abstract) and the Task Force on Sudden Cardiac Death of the European Society of
Cardiology link
Note: Guideline withdraw
- ^ a
b Sherrid MV, Barac I, McKenna WJ, Eliott M, Dickie
S, Chojnowska L, Casey S, Maron BJ. Multicenter study of the efficacy and safety of disopyramide in obstructive hypertrophic
cardiomyopathy. J Am College of Cardiol 2005; 45:1251–58
- ^ Wynne J, Braunwald E.
Hypertrophic cardiomyopathy. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular medicine. 5th ed. Philadelphia: WB
Saunders; 1997.
- ^ Morrow AF. Hypertrophic subaortic stenosis. Operative
methods utilized to relieve left ventricular outflow obstruction. J Thorac Cardiovasc Surg
1978; 76:423–30
- ^
Nakatani S, Schwammenthal E, Lever HM, Levine RA, Lytle BW, Thomas JD. New insights into the reduction of mitral valve systolic
anterior motion after ventricular septal myectomy in hypertrophic obstructive cardiomyopathy. Am
Heart J 1996; 131:294–300
- ^ a b Balaram SK, Sherrid MV, DeRose JJ, Hillel Z, Winson G,
Swistel DG. Beyond extended myectomy for hypertrophic cardiomyopathy: The RPR (Resection–Plication–Release) Repair.
Annals of Thoracic Surgery 2005; 80:217–23
- ^ McIntosh CL, Maron
BJ, Cannon RO, Klues H. Initial results of combined anterior mitral valve plication and ventricular septal myotomy–myectomy for
relief of left ventricular outflow obstruction in patients with hypertrophic cardiomyopathy. Circulation 1992; 86:II 60–7
- ^ Brilakis ES,
Nishimura RA. Severe pulmonary hypertension in a patient with hypertrophic cardiomyopathy: response to alcohol septal ablation.
Heart. 2003 Jul; 89(7):790. (Medline abstract)
- ^ Ommen SR,
Nishimura RA, Squires RW, Schaff HV, Danielson GK, Tajik AJ. Comparison of dual-chamber pacing versus septal myectomy for the
treatment of patients with hypertropic obstructive cardiomyopathy: a comparison of objective hemodynamic and exercise end points.
J Am Coll Cardiol. 1999 Jul; 34(1):191–6. (Medline abstract)
- ^ Kittleson M, Meurs K, Munro M, Kittleson J, Liu S, Pion P, Towbin J (1999). "Familial hypertrophic
cardiomyopathy in maine coon cats: an animal model of human disease". Circulation 99 (24): 3172-80. PMID
10377082.
- ^ Meurs K, Sanchez X, David R, Bowles N, Towbin J, Reiser P, Kittleson J, Munro M, Dryburgh K, Macdonald K,
Kittleson M (2005). "A cardiac myosin binding protein C mutation in the Maine Coon cat with familial hypertrophic
cardiomyopathy". Hum Mol Genet 14 (23): 3587-93. PMID 16236761.
- ^ Veterinary Cardiac Genetics Laboratory of the College of Veterinary Medicine
External links
|
Circulatory system pathology (I, 390-459) |
| Hypertension |
Hypertensive heart
disease - Hypertensive nephropathy - Secondary hypertension (Renovascular
hypertension) |
| Ischaemic heart disease |
Angina
pectoris (Prinzmetal's angina) - Myocardial infarction - Dressler's syndrome |
| Pulmonary circulation |
Pulmonary embolism
- Cor pulmonale |
| Pericardium |
Pericarditis - Pericardial effusion - Cardiac tamponade |
| Endocardium/heart valves |
Endocarditis -
mitral valves (regurgitation,
prolapse, stenosis) - aortic valves (stenosis, insufficiency) - pulmonary valves (stenosis, insufficiency) -
tricuspid valves (stenosis,
insufficiency) |
| Myocardium |
Myocarditis - Cardiomyopathy (Dilated cardiomyopathy, Hypertrophic cardiomyopathy,
Loeffler endocarditis, Restrictive
cardiomyopathy) - Arrhythmogenic right ventricular
dysplasia |
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(Supraventricular, AV
nodal reentrant, Ventricular) - Atrial
flutter - Atrial fibrillation - Ventricular fibrillation - Premature contraction (Atrial, Ventricular) -
Sick sinus syndrome |
| Other heart conditions |
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| Cerebrovascular diseases |
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Subdural hemorrhage, Subarachnoid
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| See also congenital (Q20-Q28, 745-747) |
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