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PubMed2000

Local intraarterial fibrinolytic therapy for embolic stroke associated with vascular anomalies--two case reports.

Two cases of embolic stroke associated with vascular anomalies were treated by intraarterial fibrinolytic therapy. A 78-year-old male had embolic stroke associated with fenestration of the middle cerebral artery (MCA). The embolus lodged in the terminal portion of the right internal carotid artery (ICA) and in the M2 portion of the right MCA. The fenestration was not detected before local fibrinolytic therapy, but was identified by postinterventional angiography. An 82-year-old female had a left-sided persistent primitive trigeminal artery (PPTA), and the embolus lodged in the terminal portion of the left ICA. Left internal carotid angiography also showed rich collateral circulation via the abundant leptomeningeal anastomosis. The PPTA involved the left ICA, so the anomalous anatomy had to be considered in performing local thrombolysis. However, the rich collateral circulation allowed recanalization of the occluded ICA without inducing bleeding. Dissolution of persistently adherent emboli must be performed with great care because of the possibility of such rare vascular anomalies.

Aged↗
PubMed2002

Neuroprotective effects of the spin trap agent disodium-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (generic NXY-059) in a rabbit small clot embolic stroke model: combination studies with the thrombolytic tissue plasminogen activator.

BACKGROUND AND PURPOSE: It has been proposed that the novel spin trap agent disodium-[(tert-butylimino)methyl]benzene-1,3-disulfonate N-oxide (NXY-059) may be useful in the treatment of ischemic stroke. However, there is little information concerning the neuroprotective properties of NXY-059 when administered after an embolic stroke. Moreover, there is no information available concerning the combination of NXY-059 with the only Food and Drug Administration-approved pharmacological agent for the treatment of acute stroke, the thrombolytic tissue plasminogen activator (tPA). Thus, we determined the effects of NXY-059G, a generic form of NXY-059, on behavioral outcome after an embolic stroke when administered alone or in combination with tPA. METHODS: Male New Zealand White rabbits were embolized by injecting a suspension of small blood clots into cerebral circulation via a carotid catheter. NXY-059G (100 mg/kg) was infused intravenously 5 minutes or 3 hours after embolization, whereas control rabbits received infusions of the saline vehicle. In tPA studies, the thrombolytic was administered intravenously starting 60 minutes or 3 hours after embolization (3.3 mg/kg). In combination studies, NXY-059G was given 5 minutes after embolization, followed by the administration of tPA beginning either 60 minutes or 3 hours after embolization. Behavioral analysis was conducted 24 hours after embolization. RESULTS: In the vehicle control group, the ES50 value (calculated as the amount of microclots [milligrams] that produce neurological dysfunction [impairment] in 50% of the rabbits within a specific treatment group) measured 24 hours after embolism was 1.04+/-0.31 mg, and this was increased by 153% to 2.54+/-0.72 mg if NXY-059G was administered beginning 5 minutes after embolization. However, if NXY-059G was administered beginning 3 hours after embolization, the ES50 was 2.01+/-0.40 mg. The rabbits treated with tPA alone had an ES50 of 2.64+/-0.66 or 0.63+/-0.35 mg if tPA administration started 60 minutes or 3 hours after embolization, respectively. If tPA was administered after NXY-059G (started at 5 minutes), the ES50 values were 3.15+/-0.50 or 2.66+/-0.82 if tPA administration started 60 minutes or 3 hours after embolization, respectively. CONCLUSIONS: This study suggests that NXY-059G is neuroprotective and can increase behavioral ratings if administered early after an embolic stroke. In addition, the study shows that NXY-059G can be used in combination with tPA without negative side effects. The drug combination can improve behavioral function and increase ES50 values. However, during the short time course of the behavioral analysis, the combination was not statistically better than either drug alone.

Animals↗
PubMed1991

Perioperative stroke. Part II: Cardiac surgery and cardiogenic embolic stroke.

The major mechanism of stroke in cardiac surgery is embolization. The risk is higher in intracardiac than in extracardiac surgery. The incidence of stoke associated with CABG is about 5%. The cerebral protective properties of isoflurane and thiopentone, acid-base management, and monitoring of cerebral perfusion during cardiopulmonary bypass are discussed. Prophylactic carotid endarterectomy for patients with asymptomatic carotid disease before cardiac surgery is not necessary. Symptomatic carotid disease increases the risk of stroke, and the management of patients who have both symptomatic coronary and carotid artery diseases is discussed. Cardiogenic embolism is probably responsible for many perioperative strokes. Patients with atrial fibrillation, valvular disease, and prosthetic heart valves are at high risk of cardiogenic embolism. Strokes associated with cardioversion, pacemaker insertion, coronary arteriography and angioplasty are explored.

Cardiac Surgical Procedures↗
PubMed2004

Group B streptococcus endogenous endophthalmitis presenting as septic arthritis and a homonymous hemianopsia due to embolic stroke.

PURPOSE: To report a case of group B streptococcus (GBS) endogenous endophthalmitis in a patient presenting with septic arthritis and a homonymous hemianopsia due to embolic stroke. DESIGN: Observational case report. METHODS: A 75-year-old woman with septic arthritis and a homonymous hemianopsia due to embolic stroke was examined and found to have endogenous GBS endophthalmitis due to bacterial endocarditis. RESULTS: Magnetic resonance imaging showed many septic emboli to the brain, including the left occipital lobe. Fundus examination showed evidence for endogenous endophthalmitis. Blood and urine cultures were positive for GBS. A mitral valve vegetation was presumed to be the cause of the intracranial septic emboli and was demonstrated on transesophageal echocardiography. CONCLUSIONS: Septic arthritis and embolic stroke are suggestive of endocarditis and sepsis. Endogenous endophthalmitis in this case led to transesophageal echocardiography, which was diagnostic for endocarditis.

Aged↗
PubMed1991

Factors relevant to preventing embolic stroke in patients with non-rheumatic atrial fibrillation.

Whether or not to treat patients with non-rheumatic atrial fibrillation with anticoagulants to prevent embolic stroke is a dilemma for physicians. If randomized trials, currently underway, demonstrate a beneficial effect, the dilemma will not be solved because not all of the relevant factors can be addressed by trials. We used current knowledge about non-rheumatic atrial fibrillation and a method of obtaining patient-derived weights for avoiding stroke from eight medically trained subjects, to determine the overall benefit of anticoagulants and to see what factors were relevant and what effect each might have in deciding whether to use anticoagulant therapy. Using standard assumptions, anticoagulants gave an expected benefit for all subjects. The expected benefit (expressed in terms of lives per 1000 saved due to anticoagulants) varied between 5.4 and 46.7. This benefit remained for all subjects when we did a sensitivity analysis for different rates of stroke prevented by anticoagulants and different rates of intracranial hemorrhage caused by anticoagulants. When we used different baseline rates of stroke and different impacts of major hemorrhagic complications the benefit disappeared for 3 and 4 subjects respectively. We found the factors that were most crucial to the decision will not be included in randomized trials; the weight that an individual would place on avoiding embolic stroke vs the risk of intracranial bleeding from anticoagulant therapy; and the rate of embolic stroke that could be expected for the subject at risk. Factors which will be measured in randomized trials, will change results less substantially: the increased risk of major hemorrhages; the proportion of strokes that could be prevented by treatment; the increase in risk of intracranial hemorrhage. This method of analysis suggests that for most patients anticoagulants are beneficial and that the most important factor in determining this result is the value that subjects put on different outcomes.

Adult↗
PubMed1994

Effect of delayed thrombolysis with rt-PA in a rat embolic stroke model.

The effect of delayed thrombolysis with recombinant tissue plasminogen activator was tested in an embolic stroke model. The carotid territory was embolized in 103 rats with fibrin-rich clots formed and washed in polyethylene tubes. Hemispheric cerebral blood flow before and after embolization was measured by the intra arterial 133Xe injection method. At five delay times, 15-240 min after embolization, 69 animals were treated with tissue plasminogen activator, 20 mg/kg, and 34 animals with saline. Carotid angiography displayed the grade of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed after 2 days, evaluated neuropathologically, and infarct volume measured. Cerebral blood flow was reduced by 56-71% after embolization. Reperfusion induced by thrombolytic therapy was demonstrated by comparing the posttreatment angiography of the pooled five treatment groups to control animals. Thrombolytic therapy significantly reduced the infarct volume and improved the prekill clinical score by up to 2 h of treatment delay, and treatment might have been beneficial even after 4 h delay. Prolonging the delay of treatment increased the infarct volume (p < 0.001, Jonck-heere-Terpstra test). Only a few hemorrhagic complications were observed. Thus, thrombolytic therapy in embolic stroke induced recanalization. The effect on clinical outcome and infarct volume was dependent on delay time.

Animals↗
PubMed2005

Early prediction of gross hemorrhagic transformation by noncontrast agent MRI cluster analysis after embolic stroke in rat.

BACKGROUND AND PURPOSE: Our goal was to develop magnetic resonance indices, without image contrast agent enhancement, that predict hemorrhagic transformation (HT) in a rat model of embolic stroke. METHODS: Male Wistar rats subjected to embolic stroke with (n=12) or without (n=10) the combination treatment with recombinant tissue plasminogen activator and an anti-platelet glycoprotein IIb/IIIa antibody 7E3 F(ab')2 initiated at 4 hours after onset of stroke were investigated using a 7-T MRI system. Radiofrequency saturation T1 (T1sat) maps with magnetization transfer, apparent diffusion coefficient of water (ADCw) maps in 3 directions, and T2 maps were measured at 2, 24, and 48 hours after embolization. MRI data were analyzed individually and using 2D cluster plots. Histological measurements were obtained at 48 hours. RESULTS: Gross hemorrhage was detected at 48 hours in 7 (4 control, 3 treated) of 22 animals. The 2D cluster plot using MRI T1sat and ADCw maps obtained at 2 hours after stroke predicted all gross HT. The location of gross hemorrhage predicted by the 2D cluster plot was within 0.75 mm of the identifying MRI cluster. CONCLUSIONS: The 2D MRI cluster plot analysis using T1sat and ADCw maps acquired at 2 hours after the onset of embolic stroke predicts gross HT.

Animals↗
PubMed2005

Map-ISODATA demarcates regional response to combination rt-PA and 7E3 F(ab')2 treatment of embolic stroke in the rat.

PURPOSE: To investigate the ability of map-ISODATA (Iterative Self-Organizing Data Analysis Technique) to classify the different categories of ischemic damage in the lesion and to evaluate a combined (thrombolysis plus antiplatelet) treatment efficacy in an embolic stroke of rat. MATERIALS AND METHODS: Rats subjected to embolic stroke with (N=12) and without (N=10) rt-PA and 7E3 F(ab')2 treatment (4 hours after embolization) were followed (at 2, 24, and 48 hours post-MCAO) with magnetic resonance imaging (MRI) using T1, T2, and apparent diffusion coefficient of water (ADCw). ISODATA was computed from T1, T2, and ADCw maps. The signatures characterized by the map-ISODATA were compared with histological quantitative evaluation and were employed to demarcate the specific regions in the lesion. RESULTS: The signature described by map-ISODATA is highly correlated with the degree of tissue damage in the lesion and can distinguish the severity of ischemic tissue injury. Based upon map-ISODATA, ischemic lesion area can be divided into three specific regions, each characterized by a distinct evolution of injury and treatment response. The combined treatment significantly reduces the lesion size between 24 and 48 hours and improves the outcome 48 hours post-MCAO compared with the control group. CONCLUSION: Map-ISODATA provides an accurate means to identify lesion area, to distinguish ischemic damage, and to detect treatment response. 7E3 F(ab')2 extends the rt-PA treatment window to at least four hours after the onset of embolic stroke of rat.

Analysis of Variance↗
PubMed1992

[Atrial septal defects and embolic stroke in young adults].

The mechanism of embolic stroke in young adults remains unidentified in about 35% of cases. In recent years defects in the atrial septum have been described as an important route for cerebral and retinal embolism. These include classical atrial septal defect and patent foramen ovale, as well as the less well-recognized entity of atrial septal aneurysm, with or without interatrial communication. The combined incidence of these defects in the general population is between 20-35%. The introduction of transesophageal echocardiography and the use of echogenic contrast have lead to significant improvement in identification. We describe 3 patients in whom atrial defects were identified as possible routes for cerebral embolism: The first presented with recurrent stroke and combined atrial septal aneurysm and patent foramen ovale. In the second, patent foramen ovale was found in a patient with 2 prosthetic values. The third was a soldier in whom patent foramen ovale was found following transient loss of consciousness. Based on our modest experience and review of the literature we believe that transesophageal and contrast echocardiography should be performed in every young patient with unexplained cerebral ischemia.

Adult↗
PubMed1992

Reduction of infarct volume and mortality by thrombolysis in a rat embolic stroke model.

BACKGROUND AND PURPOSE: Thrombolytic therapy with recombinant tissue plasminogen activator was tested in a rat embolic stroke model. METHODS: The rat carotid territory was embolized with arterial-like microthrombi formed under pressure. Hemispheric cerebral blood flow before and after embolization was measured by the intraarterial Xenon-133 injection method. Fifteen minutes after embolization, 24 rats were treated with 3 mg/kg or 10 mg/kg tissue plasminogen activator, and 27 were treated with saline. Carotid angiography displayed the rate of occlusion of the cerebral arterial supply before and after treatment. Brains were fixed and evaluated neuropathologically and infarct volume was measured. RESULTS: Cerebral blood flow was reduced 70-86% after embolization. The comparison of pretreatment and posttreatment angiography showed significant (p = 0.0005) reperfusion in the treated rats. Thrombolytic therapy significantly reduced the infarct volume from 55.1% to 24.4% of embolized hemisphere volume (p = 0.007) and increased the survival rate from 0.48 to 0.96 (p = 0.0004). Fifty-three percent of the embolized rats recanalized completely after thrombolytic treatment and developed almost no infarction (median volume 2.8%), and all survived. No hemorrhagic complications were observed. CONCLUSIONS: Early thrombolytic therapy induced recanalization and reduced mortality and infarct volume after embolic stroke in this model.

Animals↗
PubMed2000

Magnetic resonance imaging indexes of therapeutic efficacy of recombinant tissue plasminogen activator treatment of rat at 1 and 4 hours after embolic stroke.

With use of magnetic resonance imaging (MRI), the effects of early and delayed treatment of embolic stroke in rat with recombinant tissue plasminogen activator (rt-PA) were investigated. Rats with embolic stroke were treated with rt-PA at 1 (n = 9) or 4 (n = 7) hours after stroke onset or were untreated (n = 15). Diffusion-weighted imaging, perfusion-weighted imaging, and T2-weighted imaging were performed before and after embolization from 1 hour to 7 days. No significant differences were detected in the relative areas with low cerebral blood flow (CBF), apparent diffusion coefficient of water (ADCw), and T2 between the 4-hour treated group and the untreated group. Significant decreases in the average relative areas with low CBF were detected in the 1-hour treated group from 4 to 48 hours after embolization as compared with the untreated group. The increase in T2 in the 1-hour treated group was significantly lower than in the untreated and 4-hour treated groups. A significant increase in ADCw was detected in the 1-hour treated group at 3 and 24 hours after embolization as compared with the untreated and 4-hour treated groups. Secondary embolization was detected by both MRI and laser scanning confocal microscopy. The data suggest that MRI can detect the efficacy of rt-PA treatment and secondary ischemic damage.

Animals↗
PubMed2000

Mitral papillary fibroelastoma as a cause of cardiogenic embolic stroke: report of two cases and review of the literature.

UNLABELLED: Papillary fibroelastoma (PFE) is a rare benign tumour that attaches to the endocardial surface, mostly on cardiac valves. Though usually asymptomatic, it can be the source of several complications. To date, 49 cases have been reported of embolic stroke with a PFE as the probable origin. CASE REPORTS: (i) a 39-year-old male presented with ischemic embolic stroke; the presence of a PFE was assessed by means of transoesophageal echocardiography and confirmed by pathological findings; (ii) a 32-year-old woman presented with sudden onset of left hemiparesis; a cardiogenic embolic stroke was suspected, and a diagnosis of PFE was made based on echocardiographic and pathological findings. In both cases, surgical excision of the tumours was performed with no recurrences at follow-up. Two mechanisms can explain the formation of emboli in PFE: dislodgement of the tumour leaves or fibrin-platelet aggregation on the endocardial surface of these leaves. Transthoracic echocardiography may lead to the suspicion of a PFE, but transoesophageal echocardiography is required for confirmation. Prompt surgical excision is indicated in most cases. Anticoagulation is only recommended in situations of high surgical risk and during the wait for surgery.

Adult↗
PubMed1989

Evaluation of recombinant tissue plasminogen activator in embolic stroke.

In an effort to determine the value of tissue-type plasminogen activator (TPA) in the treatment of embolic stroke, 17 rabbits were subjected to a model of embolic stroke in which 2-hour-old, tin-impregnated, autologous clots were embolized to the bifurcation of the internal carotid artery at the circle of Willis via retrograde injection into the cannulated external carotid artery. High-resolution digital subtraction radiography was used to localize clots intracranially at the carotid bifurcation. Circulation through the internal carotid artery and intracranial vessels was monitored with serial digital subtraction angiography before and after embolization and during treatment. Disappearance of the tin marker on the digital subtraction radiograph indicated dissolution of clot and was associated with reestablishment of circulation on the digital subtraction angiogram. Experimental animals were treated with human-specific recombinant TPA 30 minutes, 2 hours, or 4 hours after clot embolization. TPA was administered as an intravenous bolus of 0.5 mg/kg followed by an infusion of 1 mg/kg/h for 2 hours. Digital subtraction angiograms were performed every 30 minutes. All clots dissolved, and cerebral circulation was reestablished within 120 minutes of treatment. In control animals treated with saline, embolized clots were stable, and the internal carotid artery remained occluded. At the completion of each study, the animal was perfused with freshly prepared, buffered 2,3,5-triphenyltetrazolium chloride (TTC) for demarcation of cerebral infarction. Control animals demonstrated infarction of 50 +/- 3.6% of the ipsilateral cerebral hemisphere, with an infarct weight of 2.1 +/- 0.2 g.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Multiparametric ISODATA analysis of embolic stroke and rt-PA intervention in rat.

To increase the sensitivity of MRI parameters to detect tissue damage of ischemic stroke, an unsupervised analysis method, Iterative Self-Organizing Data Analysis Technique Algorithm (ISODATA), was applied to analyze the temporal evolution of ischemic damage in a focal embolic cerebral ischemia model in rat with and without recombinant tissue plasminogen activator (rt-PA) treatment. Male Wistar rats subjected to embolic stroke were investigated using a 7-T MRI system. Rats were randomized into control (n=9) and treated (n=9) groups. The treated rats received rt-PA via a femoral vein at 4 h after onset of embolic ischemia. ISODATA analysis employed parametric maps or weighted images (T1, T2, and diffusion). ISODATA results with parametric maps are superior to ISODATA with weighted images, and both of them were highly correlated with the infarction size measured from the corresponding histological section. At 24 h after embolic stroke, the average map ISODATA lesion sizes were 37.7+/-7.0 and 39.2+/-5.6 mm2 for the treated and the control group, respectively. Average histological infarction areas were 37.9+/-7.4 mm2 for treated rats and 39.4+/-6.1 mm2 for controls. The R2 values of the linear correlation between map ISODATA and histological data were 0.98 and 0.96 for treated and control rats, respectively. Both histological and map ISODATA data suggest that there is no significant difference in infarction area between non-treated and rt-PA-treated rats when treatment was administered 4 h after the onset of embolic stroke. The ISODATA lesion size analysis was also sensitive to changes of lesion size during acute and subacute stages of stroke. Our data demonstrate that the multiparameter map ISODATA approach provides a more sensitive quantitation of the ischemic lesion at all time points than image ISODATA and single MRI parametric analysis using T1, T2 or ADCw.

Algorithms↗
PubMed1987

A model for quantitative evaluation of embolic stroke therapy.

We developed a small animal embolic stroke model for pharmacological screening trials. Microspheres are injected into the carotid circulations and group embolus dose-response relationships are calculated. Emboli quantity is related to neurologic injury, and small changes in neurologic function are detectable. Rabbits tolerated twice as many microspheres when cyproheptadine-treated after embolization. This demonstrated both the sensitivity of the model and the value of serotonin antagonists in reducing neurological injury.

Animals↗
PubMed1996

Embolic stroke after ligation of the pulmonary artery in patients with functional single ventricle.

In the setting of functional single ventricle with pulmonary overcirculation, pulmonary artery banding is frequently used to alleviate symptoms and to prepare for staged repair. At subsequent cavopulmonary anastomosis or Fontan procedure, the pulmonary artery may be ligated at the site of the pulmonary band. This article describes the association of embolic stroke and thrombus in a ligated or divided pulmonary artery stump in three patients with functional single ventricle. These events occurred from 1990 through 1992 among the 1700 inpatient pediatric cardiology admissions at two institutions. The patients, ranging in age from 15 months to 9 years, had cerebral infarctions documented by computed axial tomography scan or magnetic resonance imaging associated with the echocardiographic finding of thrombus in the proximal pulmonary artery stump after the embolic strokes. The strokes occurred 5 days to 5 years after surgery. Two patients had a second infarction within 2 to 5 weeks of the initial stroke. It is concluded that the presence of the ligated pulmonary artery stump may place patients at risk for embolic stroke. Surgical approaches to reduce the risk of thrombus formation should be considered prospectively in this patient group.

Cerebral Infarction↗
PubMedDate not supplied

Immediate anticoagulation of embolic stroke: brain hemorrhage and management options. Cerebral Embolism Study Group.

The clinical implications of hemorrhagic transformation of embolic brain infarction were explored by studying 30 patients with cardiogenic brain embolism and either hemorrhagic infarct (HI) or intracerebral hematoma (ICH) on CT. At the time of identification of hemorrhage, 19 patients were receiving anticoagulants and 11 were not. Eight anticoagulated patients and three nonanticoagulated patients developed late HI without attendant worsening after an initial CT was nonhemorrhagic. Hemorrhagic transformation without worsening most often occurred after 12 hours but before 48 hours following stroke onset and was associated with large infarcts (82%) but not with age, blood pressure or embolic source. Seven anticoagulated patients, six with large infarcts, and one nonanticoagulated patient with a small infarct abruptly worsened from eight hours to 11 days after stroke, with CT revealing ICH or severe HI. Excessive anticoagulation or acute hypertension potentially contributed to hemorrhagic transformation in four of five patients who were receiving heparin. Brain hemorrhage in embolic strokes most often occurs with large infarcts. Early CT may not allow the identification of large embolic infarcts that are destined to later undergo spontaneous hemorrhagic transformation. For large embolic infarcts, a delay of several days before anticoagulation and special efforts to avoid excessive anticoagulation and hypertension may be prudent. The initial administration of large, bolus doses of heparin should perhaps be avoided.

Adult↗
PubMed2005

Risk factors for first-ever acute ischemic non-embolic stroke in elderly individuals.

BACKGROUND: Stroke is a leading cause of mortality and subsequent serious long-term physical and mental disability among survivors. In the elderly, ischemic stroke accounts for more than 80% of all strokes. OBJECTIVES: To identify major risk factors for a first-ever acute ischemic/non-embolic stroke in individuals older than 70 years. METHODS: A population-based case-control study of patients admitted to the University Hospital of Ioannina, Epirus, Greece, due to first-ever ischemic/non-embolic stroke from March 1997 to January 2002. All patients were subjected to brain CT and had their serum lipids and biochemical metabolic parameters determined within 24 h from the onset of symptoms. RESULTS: A total of 163 (aged>70 years) consecutive stroke patients and 166 apparently healthy volunteers were studied. An atherogenic lipid profile and metabolic disturbances were more prevalent in the patient group than in stroke-free controls. Multivariate logistic regression analysis identified diabetes mellitus (odds ratio (OR), 1.92; 95% CI, 1.02-3.63), triglycerides (TG) (OR, 1.16; 95% CI, 1.09-1.22), HDL-cholesterol (OR, 0.57; 95% CI, 0.43-0.76), apo A-I (OR, 0.80; 95% CI, 0.70-0.92), lipoprotein(a) [LP(a)] (OR, 1.51; 95% CI, 1.25-1.79), uric acid (OR, 1.30; 95% CI, 1.06-1.59) albumin (OR, 0.38; 95% CI, 0.20-0.70) fibrinogen (OR, 1.10; 95% CI, 1.05-1.13) and the metabolic syndrome (OR 2.48, 95% CI, 1.16-5.29) as significantly associated with ischemic/non-embolic stroke. CONCLUSION: Ischemic non-embolic stroke in the elderly is associated with dyslipidemia and several predictor metabolic factors, which could be substantially modified by lifestyle changes and therapeutic intervention.

Acute Disease↗