Background

Angina pectoris (AP) represents the clinical

syndrome occurring when myocardial oxygen
demand exceeds supply. The term is derived from
Latin; the literal meaning is "the choking of the
chest;" angere, meaning "to choke" and pectus,
meaning "chest." The first English-written account
of recurrent angina pectoris was by English
nobleman Edward Hyde, Earl of Clarendon. He
described his father as having, with exertion, "a
pain in the left armso much that the torment
made him pale".[1] The first description of angina
as a medical disorder came from William
Heberden. Heberden, a prodigious physician, made
many noteworthy contributions to medicine during
his career. He presented his observations on "dolor
pectoris" to the Royal College of Physicians in
1768. Much of his classic description retains its
validity today.[2]

Angina pectoris has a wide range of clinical
expressions. The symptoms most often associated
to angina pectoris are substernal chest pressure or
tightening, frequently with radiating pain to the
arms, shoulders, or jaw. The symptoms may also be
associated with shortness of breath, nausea, or
diaphoresis. Symptoms stem from inadequate
oxygen delivery to myocardial tissue. No definitive
diagnostic tools that capture all patients with
angina pectoris exist. This, combined with its
varied clinical expression, makes angina pectoris a
distinct clinical challenge to the emergency
physician. The disease state can manifest itself in a
variety of forms:

Stable angina pectoris is classified as a
reproducible pattern of anginal symptoms that
occur during states of increased exertion.
Unstable angina pectoris (UA) manifests either as
an increasing frequency of symptoms or as
symptoms occurring at rest.
Prinzmetal angina or variant angina occurs as a
result of transient coronary artery spasms. These
spasms can occur either at rest or with exertion.
Unlike stable or unstable angina, no pathological
plaque or deposition is present within the coronary
arteries that elicits the presentation. On
angiography, the coronary arteries are normal in
appearance with spasm on angiography.
Cardiac syndrome X occurs when a patient has all
of the symptoms of angina pectoris without
fundal
Angin pectoral ( AP ) reprezint sindrom clinic
care apar atunci cnd cererea de oxigen miocardic
depete oferta . Termenul este derivat din limba
latin , sensul literal este "sufocare a pieptului , " " .
Piept " angere , care nseamn "a sufoca " i pectus
, ceea ce nseamn Primul cont englez - scris de
angina pectorala recurente a fost de limba englez
nobil Edward Hyde , conte de Clarendon . El a
descris tatl su ca avnd , cu efort , " o durere n
braul stng ... att de mult nct chin fcut s
plesc " . [ 1 ] Prima descriere a anginei ca o
afectiune medicala a venit de la William Heberden
. Heberden , un medic prodigioas , a fcut
numeroase contribuii notabile la medicament n
timpul carierei sale . El a prezentat observaiile sale
cu privire la " angina dolor ", la Colegiul Regal al
Medicilor din 1768 . O mare parte din descrierea
lui clasic pstreaz valabilitatea i n prezent . [ 2 ]

Angin pectoral are o gam larg de expresii
clinice . Simptomele cele mai des asociate cu
angin pectoral sunt sub presiune retrosternale sau
strngere , frecvent cu dureri radiante n brae ,
umeri , sau maxilarului . Aceste simptome pot fi ,
de asemenea, asociate cu dificultati de respiratie ,
greata sau diaforeza . Simptomele provin de la
livrare de oxigen inadecvat a tesutului miocardic .
Nu sunt instrumente de diagnosticare definitive
care surprind toi pacienii cu angin pectoral
exista . Acest lucru , combinat cu expresia ei
variate clinice , face angin pectoral o provocare
clinic distinct pentrumedic de urgenta . Stare de
boal se poate manifesta ntr -o varietate de forme :

Angina pectorala stabila este clasificat ca un model
reproductibil de simptome anginoase care apar n
timpul strilor de efort crescut .
Angin pectoral instabil ( UA ) manifest , fie ca
o frecven tot mai mare de simptome sau
simptome care apar in repaus .
Angin Prinzmetal sau angina variant apare ca un
rezultat al spasmelor arterelor coronare tranzitorii .
Aceste spasme poate aprea fie n repaus sau la
efort fizic . Spre deosebire de angina pectorala
stabila sau instabila , nu placa patologice sau
depunerea este prezent in arterele coronare care
elicitsprezentare . Pe angiografie , arterele coronare
sunt normale n aparen cu spasme la angiografie .
Cardiac Sindromul X se produce atunci cnd un
pacient are toate simptomele de angina pectorala ,
coronary artery disease or spasm.
Pathophysiology
The past 2 decades has greatly expanded our
overall understanding of the pathophysiology of
myocardial ischemic syndromes. The primary
dysfunction in angina pectoris is decreased oxygen
delivery to myocardial muscle cells. The 2
predominant mechanisms by which delivery is
impaired appear to be coronary artery narrowing
and endothelial dysfunction. Any other mechanism
that affects oxygen delivery can also precipitate
symptoms.

Extracardiac causes of angina include, but are by
no means limited to, anemia, hypoxia, hypotension,
bradycardia, carbon monoxide exposure, and
inflammatory disorders.[3] The end result is a shift
to anaerobic metabolism in the myocardial cells.
This is followed by a stimulation of pain receptors
that innervate the heart. These pain receptors
ultimately are referred to afferent pathways, which
are carried in multiple nerve roots from C7 through
T4. The referred/radiating pain of angina pectoris is
believed to occur because these afferent pathways
also carry pain fibers from other regions (eg, the
arm, neck, and shoulders).

Coronary artery narrowing
Coronary artery narrowing appears to be the
etiology of cardiac ischemia in the preponderance
of cases. This has clinical significance when
atherosclerotic disease diminishes or halts blood
flow through the coronary arterial circulation,
interfering with normal laminar blood flow. The
significance of even a small change in the diameter
of a blood vessel can be profound. The Poiseuille
law predicts this outcomethe rate of flow is
decreased exponentially by any change in the
radius of the lumen. As with a smaller pediatric
airway, even relatively minute changes in diameter
have dramatic consequences in flow rates. Thus,
when a lumen is narrowed by one fifth, the flow
rate is decreased by about one half. This predicts
that even a small change in a coronary artery
plaque size can affect the oxygenation through that
vessel's territory.

The epicardial vessel, where atherosclerosis often
takes place, has the capacity to dilate via
autoregulatory mechanisms to respond to increased
demand. Angina occurs as this compensatory
fara boala coronariana sau spasm .
Fiziopatologie
n ultimele dou decenii, sa dezvoltat foarte mult
intelegerea noastra de ansamblu a fiziopatologia de
sindroame cardiace ischemice . Disfuncie primar
n angina pectoral este redus de livrare de oxigen
la celulele musculare miocardice . Cele dou
mecanisme predominant n care livrarea este
afectata par a fi ingustarea arterelor coronare si
disfunctia endoteliala . Orice alt mecanism care
afecteaz de livrare de oxigen poate precipita , de
asemenea, simptome .

Cauze extracardiace de angina pectorala includ ,
dar nu sunt n nici un caz limitat la , anemie ,
hipoxie , hipotensiune arterial , bradicardie ,
expunerea la monoxid de carbon , si tulburari
inflamatorii [ 3 ] Rezultatul final este o schimbare a
metabolismului anaerob n celule miocardice . .
Aceasta este urmat de o stimulare de receptori de
durere care inerveazainima . Acesti receptori de
durere in cele din urma se face referire la cai
aferente , care sunt transportate n mai multe
radacini nervoase de la C7 T4 . Menionat / dureri
radiante de angin pectoral este considerat a avea
loc , deoarece aceste cai aferente efectua, de
asemenea fibre durere de alte regiuni ( de exemplu ,
braul , gatul si umerii ) .

Ingustarea arterelor coronare
ngustarea arterei coronare pare a fietiologia
ischemie cardiac npreponderen a cazurilor .
Acest lucru are o semnificaie clinic atunci cnd
boala aterosclerotica reduce sau opreste fluxul de
sange prin intermediul circulaiei arteriale
coronariene , a interfera cu fluxul normal de snge
laminar . Semnificaia chiar o mic schimbare
ndiametrul unui vas de snge poate fi profund .
Legea Poiseuille prezice acest rezultat -rata de
curgere se micoreaz exponenial de orice
schimbare nraza delumen . Ca cu un cailor
respiratorii mici pediatru , modificri chiar i
relativ minute n diametru avea consecine
dramatice din debite . Astfel , atunci cnd un lumen
este redus cu o cincime ,debitul este redus cu
aproximativ o jumtate . Acest lucru prezice c,
chiar o mica schimbare intr-o artera dimensiune
placa coronarian poate afecta oxigenarea prin
teritoriul pe care navei.

Vasul epicardic , unde are loc adesea ateroscleroza
mechanism is overwhelmed either by large plaques
(typically considered 70% or greater obstruction) or
by significantly increased myocardial demand.[4]

Endothelial factors
Endothelial factors also play an important role in
angina pectoris. During sympathetic stimulation,
the endothelium is subjected to mediators of both
vasoconstriction and vasodilatation. Alpha-agonists
(catecholamines) directly cause vasoconstriction,
while endothelial nitrous oxide synthase creates
nitrous oxide (NO), which counteracts this
constricting force via vasodilatation.

In the diseased coronary artery, NO production is
reduced or absent. In this setting, the catecholamine
drive can overwhelm the autoregulatory
mechanisms. In addition, the endothelium of the
plaque-laden artery may, in itself, be dysfunctional.
This limits the ability of the intra-arterial
endothelium to produce mediators, which, in a
healthy artery, would protect against further
vasoconstriction, assist dilatation, and provide
protection from platelet aggregation. Small lesions
in these vessels may produce incompletely
obstructing aggregates of platelets. This would
further impede flow through the affected vessel.[4]

In the diseased heart, these 2 factors, coronary
artery narrowing and endothelial dysfunction,
synergistically result in reduced oxygen delivery to
the myocardium. The net result is angina pectoris.

Extrinsic factors
Extrinsic factors can also play a role in specific
circumstances. The oxygen-carrying capacity of
blood is based on a number of factors. The most
important of which is the amount of hemoglobin.
Any alteration in the ability of blood to carry
oxygen can precipitate angina. Anemia of any
degree can result in anginal symptoms. Given a
scenario where demand is increased, such as
climbing a flight of stairs, increased stress, or even
sexual intercourse, the anginal symptoms may
appear.[5] Abnormal hemoglobin, such as
methemoglobin, carboxyhemoglobin, or any of a
number of hemoglobinopathies, creates an
environment at greater risk for precipitating angina.

Other extrinsic factors that affect hemoglobin
formation, such as lead poisoning or iron-
, are capacitatea de a dilata prin mecanisme
autoreglatoare a rspunde cererii n cretere.
Angina apare ca acest mecanism de compensare
este copleit fie de placi mari ( de obicei
considerate de 70 % sau obstructie mai mare ) sau
prin creterea semnificativ a cererii miocardic . [ 4
]

factori endoteliale
Factorii endoteliale joac , de asemenea, un rol
important n angina pectoral . In timpul stimulare
simpatic ,endoteliul este supus mediatorii att
vasoconstricie i vasodilataie . Alfa - agoniste (
catecolamine ) produce direct vasoconstricie , n
timp ce sintetazei endoteliale de oxid de azot
creeaz oxid de azot ( NO ) , care contracareaz
aceast for constrictia prin vasodilataie .

n arterei coronare bolnave , nici o producie este
redus sau absent . n acest context , unitatea
catecolamine poate coplesi mecanismele
autoreglatoare . n plus ,endoteliul aarterei placa -
ncrcat poate , n sine , s fie disfuncional .
Acest lucru limiteaz capacitatea de endoteliul
intra- arterial pentru a produce mediatori , care ,
intr-o artera sanatoasa , ar proteja mpotriva
vasoconstricie mai mult , ajuta dilatare , i ofer o
protecie de la agregarea plachetara . Leziuni mici
din aceste nave pot produce blocarea incomplet
agregate de trombocite . Aceasta va mpiedica n
continuare debitul prinvasul afectat . [ 4 ]

n inima bolnave , aceste 2 factori , ngustarea
arterelor coronare si disfunctia endoteliala , ca
rezultat sinergic la livrare redus de oxigen la
nivelul miocardului . Rezultatul net este angina
pectoral .

factorii extrinseci
Factorii extrinseci pot juca de asemenea un rol n
circumstane specifice . Capacitatea transport
oxigenul din snge se bazeaz pe o serie de factori .
Cel mai important dintre care este cantitatea de
hemoglobina . Orice modificare n capacitatea
sngelui de a transporta oxigenul poate precipita
angina pectorala . Anemia de orice grad poate duce
la simptome anginoase . Avnd n vedere un
scenariu n cazul n care cererea este n cretere ,
cum ar fi alpinism un zbor de scri , a crescut de
stres , sau chiar actul sexual , pot aprea
simptomele anginoase . [ 5 ] hemoglobinei
deficiency states, also lead to a similar decrease in
oxygen-carrying capacity. Any mechanism that
impedes oxygen delivery to the red blood cells has
a similar effect. Therefore, any number of
pulmonary causes, such as pulmonary embolism,
pulmonary fibrosis or scarring, pneumonia, or
congestive heart failure, can exacerbate angina. A
decreased oxygen environment, such as travel to a
higher elevation, has similar consequences due to
the decrease in concentration of atmospheric
oxygen.

Variant angina
The etiology of variant angina is currently not well
understood. Research suggests that inflammatory
mediators may result in focal coronary artery
vasospasm. Another possibility is that perfusion is
decreased through microvascular circulation.
Spasm or intermittent narrowing of this
microscopic lumen may result in transient areas of
hypoperfusion and oxygen deprivation.[6]

Syndrome X
Syndrome X is the triad of angina pectoris, a
positive ECG stress test result, and a normal
coronary angiogram. The pathophysiology of this
disease is not well understood. Many theories exist
as to the underlying pathology. Decreased
oxygenation of the underlying myocardium may be
the result of impaired vasodilatation, dysfunctional
smooth muscle cells, poor or deficient
microvascular circulation, or even structural
problems on a cellular level (eg, an inappropriately
functioning sodium ion channel).[6]

Epidemiology
Frequency
United States
An estimated 6,500,000 people in the United States
experience angina pectoris.

Each year, 400,000 new cases of angina pectoris
develop.

Conservative 2006 data show 733,000 acute
coronary syndrome (ACS) discharges from
hospitals.[7]

Mortality/Morbidity
In 2005, 1 in 5 deaths is from coronary heart
disease (both angina and myocardial infarction).
anormale , cum ar fi methemoglobin ,
carboxihemoglobina , sau la oricare dintre un
numr de hemoglobinopatii , creeaz un mediu de
risc mai mare pentru precipitarea angina pectorala .

Ali factori extrinseci care afecteaz formarea
hemoglobinei , cum ar fi intoxicatia cu plumb sau
stri de deficienta de fier , de asemenea, duce la o
scdere similar n calitate de purttor de oxigen .
Orice mecanism care mpiedic livrarea de oxigen
la celule roii sanguine are un efect similar . Prin
urmare , orice numr de cauze pulmonare , cum ar
fi embolism pulmonar , fibroza pulmonara sau
cicatrici , pneumonie , sau insuficien cardiac
congestiv , poate agrava angina pectorala . Un
mediu de oxigen sczut , cum ar fi de cltorie la o
cot mai ridicat , are consecine similare ,
datoritscderii concentraiei de oxigen atmosferic .

angina varianta
Etiologia de angina varianta este n prezent nu este
bine neles . Cercetarile sugereaza ca mediatori
inflamatorii poate duce la spasmul coronarian focal
. O alt posibilitate este aceea perfuzia este redus
prin circulaie microvasculare . Spasm sau
intermitent ingustarea lumenului acest
microscopice poate duce n zone tranzitorii de
hipoperfuzie i privarea de oxigen . [ 6 ]

sindromul X
Sindromul X este triada de angina pectorala , un
ECG rezultat pozitiv la testul de stres , i un
angiografia coronariana normala . Fiziopatologia
acestei boli nu este bine neles . Exist multe teorii
pentru apatologiei de baza . Oxigenare Scderea a
miocardului care stau la baza ar putea fi rezultatul
de afectare a vasodilataie , celulele musculare
netede disfunctionale , circulatie microvasculare
sraci sau cu deficit , sau chiar probleme structurale
la nivel celular ( de exemplu , un canal inadecvat
funcioneaz ioni de sodiu ) . [ 6 ]

Epidemiologie
frecven
Statele Unite
Se estimeaza ca aproximativ 6.5 milioane de
persoane din Statele Unite experiena angin
pectoral .

n fiecare an , 400.000 de noi cazuri de angin
pectoral dezvolta .

Coronary heart disease is the single greatest killer
of American men and women.[7]

The estimated direct and indirect cost for
Americans with coronary heart disease in 2006 was
$142.5 billion.

Race
The Centers for Disease Control and Prevention
(CDC) note that the prevalence of angina and/or
coronary heart disease is highest and increasing in
Hispanics followed by whites and black non-
Hispanics (5%, 4.2%, 3.7%, respectively). This
information includes the 50 US states, the District
of Columbia, Puerto Rico, and the US Virgin
Islands.[8] [7]

Sex
Among Americans aged 40-74 years, the age-
adjusted prevalence of angina pectoris (AP) was
higher among women than men.[7] Although 2005
CDC data suggest that men (5.5%) have a higher
prevalence of angina and/or coronary heart disease
than women (3.4%).[8]


Age
The incidence of new and recurrent angina
increases with age but then declines at around 85
years.

Statistics from American Heart Association (2008
Data) and Centers for Disease Control and
Prevention.

Datele conservatoare 2006 arat 733000 sindrom
coronarian ( ACS ) deversri acute din spitale . [ 7 ]

Mortalitatea / Morbiditatea
n 2005 , 1 din 5 decese este de la boli de inima
coronariene ( atat angina pectorala si infarct
miocardic ) .

Boala coronariana este cel mai mare criminal unic
de barbati americani si femei . [ 7 ]

Costurile directe i indirecte estimate pentru
americani cu boala coronariana n 2006 a fost de
142.5 miliarde $ .

ras
La Centrul pentru Controlul si Prevenirea Bolilor (
CDC ), act de faptul c prevalena de angin
pectoral i / sau boala coronariana este cea mai
mare i n cretere n Hispanics , urmat de alb i
negru, non - Hispanics ( 5 % , 4,2 % , 3,7 % ,
respectiv ) . Aceste informaii includ cele 50 de
state din SUA , Districtul Columbia , Puerto Rico i
Insulele Virgine SUA . [ 8 ] [ 7 ]

sex
In randul americanilor in varsta de 40-74 de ani ,
prevalenta varsta ajustat de angin pectoral ( AP )
a fost mai mare in randul femeilor decat la barbati .
[ 7 ] Cu toate c date din 2005 CDC sugereaza ca
barbatii ( 5,5 % ) au o prevalenta mai mare de
angin pectoral i / sau coronariene boli de inima
decat femeile ( 3,4 % ) . [ 8 ]

vrst
Incidenta de noi i recurente angina pectorala creste
cu varsta , dar apoi scade la aproximativ 85 de ani.

Statisticile de la American Heart Association ( date
din 2008 ) i Centrele pentru Controlul si
Prevenirea Bolilor .