la morte cerebrovascolare: può presentarsi come la morte improvvisa cardiaca?
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La morte cerebrovascolare: può presentarsi come la
morte improvvisa cardiaca?
Giuseppe MicieliDip Neurologia d’Urgenza
IRCCS Istituto Neurologico Nazionale C MondinoPavia
Eleventh International SymposiumHeart Failure & Co.Morte Improvvisa
Reggia di Caserta 29-30 Aprile 2011
• After a stroke/TIA, patients are at high risk of short-term non-fatal stroke and of long-term fatal CHD• CHD is highly prevalent at autopsy in patients with stroke TIA• Recent studies confirm 10-year incidence of CHD in patients with stroke/TIA
is 20%• Secondary prevention should not only focus on the first 2-3 years• Long-term (4-5 years) secondary prevention trials (PROGRESS, SPARCL) show reduction in CHD events
Malattia cerebrovascolare: sottotipi di ictus
Albers GW et al. Chest. 1998;114:683S-698S.Rosamond WD et al. Stroke. 1999;30:736-743.
Ictus ischemico (83%)Ictus emorragico (17%)
Malattia aterotrombotica (20%)
Cardioembolismo (20%)
Patologia lacunare dei piccoli vasi (25%)
Criptogenetico e da cause rare(30%)
Emorragia intracranica (59%)
Emorragia subaracnoidea (41%)
– Mediche:• Cardiocircolatorie• Respiratorie• Infettive• Internistiche
– Neurologiche: • Stroke in evoluzione• Infarcimento emorragico• Ipertensione endocranica• Crisi epilettiche
Complicanze
Numbers and causes of death per week from stroke onset
Prosser J et al, Stroke 2007;38:2295-2302
4,5 hrs 16 hrs
TC cerebrale: ischemia cerebrale ed edema
30-day Case-Fatality Rate
Stroke type No. CFR 95%CI
Subarachnoid hemorrhage (n=118) 40 33.9% 25.4-42.4
Intracerebral hemorrhage (n=588) 284 48.3% 44.3-52.4
Cerebral ischemia (n=3594) 763 21.2% 19.9-22.5
Ill-defined events (n=53) 39 73.6% 61.7-85.5
Total (n=4353) 1126 25.9% 24.6-27.2
CFR: case-fatality rate, CI: confidence interval
L’Aquila Stroke Registry, 2004
Time interval qualifying sudden death (from symptoms)
• Up to 1 h Lie JT et al, 1975; Herzog CA et al, 2006
• Within 6 h Davies MJ et al, 1987; Corrado D et al, 1992
• Up to 24 h WHO , Sarkioja T et al, 1984; Siboni A et al, 1986
The day of the dead(1923-1924)Diego Rivera
Unexpected natural death among Korean workers (1994-1995)
Park J et al. J Occup Health 1999;41:238-243
Effects of cerebral lesions on the heart and blood pressure
Modified from Norris, 1983
64-year-old woman collapsed in the lobby of her apartment buildingCT-scan: right subdural hematoma with intracerebral right temporal and
insular hemorrhage
Baranchuk A et al. Cardiol J 2009;16:105-112
within 24 hours of admission
within 72 hours of admission
Brugada syndrome revealed by vertigo caused by cerebellar infarction (36-year-old man)
Denier C et al. Eur J Neurol 2010;17:e35-e36
Neurogenic T wave inversion in pure left stroke associated with hyperhomocysteinemia
Mandrioli J et al. JNNP 2003
admission7 days after the second stroke
Sudden cardiac arrest in a successfully embolized case of giant VA aneurysm with hydrocephalus
Mishra NK. Sur Neurol 2007;67:652-653
QT variability in CADASIL
Piccirillo G et al. Eur J Neurol 2008;15:1216-1221
Elettrocardiographic changes during central nervous system lesions
Baranchuk A et al. Cardiol J 2009;16:105-112
Neuroanatomic basis of stroke-related myocardial injury
Zhu et al, Neurology 2006
Stroke-induced sudden-autonomic death
• Role of the insular cortex in the pathophysiology of sudden death Oppenheimer et al, 1991
• Significant modulating effects of ventromedial prefrontal cortex (VMPFC) on cardiovascular responses to emotional stimuli Hiltz MJ et al. 2006
• Hemispheric dominance of sympathetic (RH) or parasympathetic (LH) activity Zamrini EY et al, 1990; Hiltz MJ et al, 2001
• Left-hemispheric inactivation increased sympathetic cardiovascular modulation; right-hemispheric inactivity furthered parasympathetic activity Hitz MJ et al, 2001
• Tailored resection of temporal lobe areas lowers sympathetic cardiovascular activation (shift towards cardiovagal predominance with possibile bradycardia or even asystole) Hiltz MJ et al 2006, Hiltz et al, 2001
Stroke-induced sudden-autonomic death
Predictors of cardiac death within 5 years after first ischemic stroke: multivariate analysis
Rincon F et al. Stroke 2008;39:2425-2431
• Infarction involving parietal lobe seem to be associated with an increased risk of cardiac events (HR 4.45 of cardiac death) Rincon et al, 2008
• Similar high risk of death after right parietal lobe infarction when infarct size is considered Rincon et al, 2008
• Probably, the parietal lobe has buffering effects on the insular region which are disinhibited after loss of parietal activity
Stroke-induced sudden-autonomic death
Cardiovascular Response after Insula Stimulation in Human Subjects
* significant difference compared with right anterior insula, p < 0.005** significant difference compared with right posterior insula, p < 0.005# significant difference compared with aggregate of right anterior and posterior insula, p < 0.005§ significant difference compared with left posterior insula, p < 0.005## significant difference compared with aggregate of left anterior and posterior insula, p < 0.005
Oppenheimer et al, 1992
Insular vs non insular involvement
Right vs Left insula
Atrial fibrillation 0.772 0.009
Sinus tachycardia HR>120 bpm
0.001 0.118
Sinus bradicardia HR<45 bpm 0.802 0.896
Atrioventricular block 0.969 0.029
Ectopic beats >10% 0.032 0.016
Prolonged QTc 0.470 0.736
ST depression 0.136 0.060
ST elevation 0.011 0.148
Inverted T wave 0.144 0.040
Isoform T wave 0.067 -
ECG abnormalities and insular involvement
Christensen et al, JNNP 2005 mod.
Two-year survival curves according to right-insular involvement
Abboud H et al, Ann Neurol 2006;59:691-699
ECG predictors for mortality among stroke cases with insular involvement
Abboud H et al, Ann Neurol 2006;59:691-699
Plasma norepinephrine concentration
Meyer S et al. Neuroreport 2004;15:357-361
Plasma epinephrine concentration
Meyer S et al. Neuroreport , 2004;15:357-361
Pathological Findings in the Heart of Patients with Brain Lesions
• Focal myocytolysis
• Myofibrillar degeneration
• Lipofuscin pigment deposition in myofibrils
• Hystocytic infiltration of the diffuse necrotic areas
Greenhoot and Reichenbach, 1969
Contraction band necrosis (coagulative myocytolysis, myofibrillar degeneration)
Fresh endocardial hemorrhage
The neurocardiac lesion: 30-year-old man died during an acute psychological stress
Intense mineralization within minutes of the onset of contraction band necrosis
Myocardial necrosis main patterns (Baroldi F, 1975): a) Coagulation necrosisb) Colliquative myocytolysisc) Coagulative myocytolysis (in reperfusion areas around regions of coagulation necrosis in transplanted heart, in sudden unexpected and accidental death, in hearts exposed to toxic levels of catecholamines)
Samuels MA. Circulation 2007;116:77-84
Cascade of events that lead to neurocardiac damage
Samuels MA, Circulation 2007;116:7784
Possible therapeutic approaches aimed to prevent neurocardiac damage
Samuels MA, Circulation 2007;116:7784
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