notes by dr Claudio Italiano
Syndrome of the sinoatrial node
coronary artery disease
Heart attack
Ischemic cardiomyopathy
Cardiac rheumatic disease
Mitral stenosis with or without atrial fibrillation
Valve prostheses
Congenital heart disease: patency of the oval foramen, mitral prolapse, etc.
Septic endocarditis
Calcification of the mitral annulus
Emboli of fat
Non-bacterial thrombotic endocarditis
Hypercoagulability conditions: neoplasms, systemic diseases, oral contraceptive
use
Atrial fibrillation
Embolism of cardiac origin causes about 15% of all strokes. The stroke caused by a heart disease is mainly due to emboli or the formation of thrombotic material on the atrial or ventricular wall, or on the left heart valves; these clots are detached and enter the arterial circulation, where they can fragment or undergo lysis with prompt restoration of the circle; alternatively, they may condition a permanent arterial occlusion and distal thrombosis may occur with obstruction resulting in disruption of the distal collateral circulation.
The emboli coming from the heart are directed more frequently towards the middle cerebral or one of its branches; rarely cause an infarct in the territory of the anterior cerebral. The emboli large enough to occlude the main portion of the middle cerebral (3-4 mm) result in a large infarct involving both the gray and white matter and a part of the cortical surface and the underlying white matter. A smaller embolo may occlude a small cortical branch or one of the penetrating branches; the location and size of the infarct also depend on the degree of sparing of the collateral circulation. Cardiogenic brain embolism is thought to occur when cardiac arrhythmias or structural abnormalities are detected or known; the most common causes of cardioembolic stroke are atrial fibrillation (FA) of non-rheumatic origin (often called "non-valvular"), myocardial infarction, valve replacement, cardiac rheumatic disease (MRC) and ischemic heart disease.
Non-rheumatic atrial fibrillation is the most common cause of brain embolism; patients with FA present an average annual risk of stroke of about 5%, although
the percentage varies depending on the presence of other risk factors such as advanced age, hypertension, reduced left ventricular function, a previous
episode of cardioembolia and diabetes mellitus. Patients younger than 60 years without any risk factor have an annual risk of about 0.5%, while those with more
factors have a risk of about 15%. The presumed stroke mechanism is the formation of thrombi in the fibrillating atrium or in the auricula, with subsequent
embolization.
-A myocardial infarction, particularly if transmural and with involvement of the anteroapical ventricular wall, is a condition at high risk of embolism,
especially in the first weeks.
- Cardiomyopathies with reduced left ventricular function are frequently associated with the formation of thrombus in the left ventricle
- Cardiac valvular prostheses, especially mechanical ones, are a common cause of cerebral embolism.
- Cardiac rheumatic disease usually causes ischemic stroke in the presence of a documentable mitral stenosis or an AF; Left atrial enlargement and congestive
heart failure are additional risk factors for the formation of atrial thrombi.
- Mitral valve prolapse can be a source of emboli; this common pathology probably causes cerebral embolism only when it is serious.
- Inborn septal defects are associated with cerebral embolism.
- Other causes, such as fat emboli, of neoplastic origin, from marital
endocarditis, of air and of amniotic fluid at the time of delivery can also,
albeit rarely, be responsible for the occurrence of a stroke.
-
Infective endocarditis causes the formation of vegetations that give rise to multiple septic emboli. The appearance of multifocal symptoms and signs in a
patient with a stroke should lead to suspicion of underlying bacterial endocarditis. Infarcts can be microscopic or large; moreover, septic emboli can
induce the formation of cerebral abscesses and mycotic aneurysms, or cause a subarachnoid hemorrhage (ESA) or cerebral hemorrhage.
The cerebral infarction may be white (non-haemorrhagic) or red (haemorrhagic). Vascular congestion is commonly of varying degree in all heart attacks, but blood supply is usually associated with embolic infarcts. Because the emboluses migrate and undergo lysis, the restoration of the circle in the infarcted brain can be associated with the appearance of petechial haemorrhages; sometimes it is observed, within the infarct area, a blood infiltration to induce a hemorrhagic infarction visible to the CT. Hemorrhagic transformation of a white infarction typically occurs 12-36 hours after embolization and is often asymptomatic. The edema invariably accompanies tissue necrosis; in smaller infarcts it may be relatively insignificant, while in larger ones a massive edema may compress the adjacent tissue, together with the ischemic process, increase the intracranial pressure and cause a brain's herniation from one compartment to another.
An embolus reaching the cerebral circulation usually manifests itself with a
focal neurological deficit with an acute onset reaching its maximum gravity from
the onset. The deficits correspond to the affected cortical areas and have
clinical characteristics similar to those of atheromatous stroke occlusion (see
the paragraphs on atherothrombotic and lacunar stroke). Some neurological
syndromes suggest an embolic origin; in the territory of the average cerebral
these include:
1) frontal opercular syndrome, in which a hyposthenia of the facial muscles is
observed and severe aphasia or dysarthria;
2) the hemiplegic syndrome of the arm or hand, in which the arm or hand is
paralyzed with or without cortical sensitive abnormalities;
3) the aphasia of Broca or Wernicke isolated;
4) the left visual hemi-inattention (see The visus) when the non-dominant
parietal lobe is involved. The acute onset of a hernia hemianopsia suggests an
embolus in the posterior cerebral, while a sudden hyposthenia of the foot and
shoulder is indicative of an embolism in the anterior cerebral; a sudden
drowsiness with an inability to direct the gaze upwards, associated with
bilateral ptosis, must lead to suspect an embolism of the apex of the basilar,
especially of the Percheron artery (it is a small artery that originates from
apex of the basilar and which irradiates both sides of the medial subtalamo and
of the thalamus).
In 3-5% of cases of cerebral infarction there is a comitial crisis at the time
of the acute event, which occurs more frequently in case of embolism rather than
thrombosis; usually crises are associated with supratentorial cortical infarcts.
3-5% of patients develop epilepsy 6-18 months after stroke and probably many
cases of idiopathic epilepsy in the elderly represent the consequence of a
silent cortical infarct
Although CT is usually negative in the first hours after an embolic stroke, this
test is able to rule out a bleeding. Later the CT scan allows to locate and
estimate the extent of the infarct and can provide elements to support the
diagnostic hypothesis of embolism, demonstrating a hemorrhagic infarction or the
presence of multiple infarcts. In any case, embolic damage may appear as a
single hypodense area compatible with an ischemic heart attack; Bleeding
petechiae within the area may not be visible as hyperdense areas because when
there is an overlap of an infarctual hypodensity, the average tissue density is
similar to that of the normal brain parenchyma. MRI is the most sensitive method
for the evaluation of embolic infarcts. Brain angiography is rarely indicated,
but when performed on the first or second day, it often documents the occlusion
of one or more vessels. Often the embolus undergoes complete lysis, so that an
angiography performed after a few days may be normal. The withdrawn liquor (see
rachicentesis) immediately after a cerebral embolism is usually normal, but the
presence of white or red blood cells makes the diagnosis of bacterial
endocarditis more likely.
Stroke therapy is the treatment of stroke itself, both in the acute and chronic
stages, as well as in preventing further embolism.
Prevention Virtually any type of heart disease is associated with an increased
risk of stroke and the best therapy of cerebral embolism is prevention;
consequently, the treatment of patients with thrombogenic cardiopathies is
always indicated.
anticoagulant therapy (cf. tao)
Some recent clinical studies have shown that anticoagulant therapy (INR 2-3) in
patients with chronic non-valvular AF (non-rheumatic) prevents brain embolism
and is risk-free. Warfarin anticoagulation reduces the risk by approximately 65%
and is generally recommended in these patients.
Patients with manifest MRC are at risk for systemic embolism and should be
treated with an anticoagulant for life; this category includes patients with
mitral stenosis, left atrial dilatation, congestive heart failure, AF, and
atrial thrombus documented on the echocardiogram.
Thromboembolism has been recognized as one of the most serious complications of
the valve prosthetic implant. In these cases anticoagulant therapy with warfarin
has been shown to be effective in preventing stroke, whereas platelet
antiplatelet therapy alone is not sufficient. In patients with prosthetic heart
valves, it is recommended to maintain a higher level of anticoagulation (INR
3,5) than those with FA.
Warfarin is more effective than acetylsalicylic acid in preventing ischemic
stroke associated with FA; however, in some patients with FA the incidence of
ischemic stroke is low and therefore treatment with warfarin is not necessary,
while others have a high risk of bleeding and, consequently, they certainly do
not benefit from anticoagulant therapy. Still others are so high at risk of
ischemic stroke that the benefits of warfarin make this drug also indicated in
the presence of a high incidence of bleeding. The use of preventive therapies is
based on the assessment of the risks and benefits related to each individual
patient. In recent years, three clinical studies have been conducted that
systematically compared acetylsalicylic acid with a placebo in preventing
cerebral infarction in patients with non-rheumatic AF. In the group of patients
undergoing antiplatelet therapy, a relative 25% reduction in stroke was observed,
compared to a 65% reduction for patients treated with warfarin. However, not all
patients with FA require warfarin therapy for stroke prevention. The Stroke
Prevention trial in Atrial Fibrillation II showed that in patients at low risk (non-hypertensive,
without recent heart failure, without previous thromboembolism) aged less than
75 years, who had been administered acetylsalicylic acid, the incidence of
thromboembolism was only 0.5% per year; therefore, treatment with
acetylsalicylic acid alone can be reasonably recommended for patients less than
75 years of age without other risk factors.
Emergency therapy is substantially comparable to that of the atherothrombotic infarction. If there is indication, the patient can undergo thrombolytic therapy. Since the emboligene source persists, at least temporarily, these patients are at risk of early embolic recurrence; for most of the causes the risk amounts to 0.5-1% per day in the first week or the first two weeks; therefore, it is advisable to start anticoagulant therapy early. Heparin, however, is generally to be avoided for about a week when the infarct is extended, since the risk of bleeding is proportional to the size of the infarct, and when the presence of bacterial endocarditis is likely. The duration of anticoagulant therapy should be determined based on the type of underlying cardiac injury and the associated risk of future embolization. If the emboligene source tends to disappear spontaneously or is treatable, anticoagulant therapy should be discontinued when the high-risk period has passed; in the case of myocardial infarction this period amounts to 2-3 months.