The exact etiology of the coronary slow flow phenomenon (CSFP) is not certain. CSFP is not a normal variant as it is an absolutely pathological entity. Furthermore, CSFP not only leads to myocardial ischemia but it can also cause classical acute ST elevation myocardial infarction, which necessitates coronary angiography for a definite diagnosis.
Anterior Wall Myocardial Infarction ; Coronary Angiography ; Myocardial Infarction ; Myocardial Ischemia ; No-Reflow Phenomenon

Distal embolization, such as plaque debris and thrombus during percutaneous coronary and carotid interventions, often lead to virtually untreatable small vessel occlusions and the no-reflow phenomenon, which may cause periprocedural end organ ischemia and infarction. This is clinically important as the one-year mortality is doubled in patients with a periprocedural myocardial infarction. To prevent a distal embolization a number of distal protection devices have been developed, with others still under development, such as a balloon occlusion device (PercuSurge GuardWire), numerous filter devices (FilterWire EX, AngioGuard, Mednova Neuroshield, AccuNet) and a catheter occlusion device (Parodi Anti-Emboli System). The usefulness and roles of distal protection devices, for cardiovascular intervention, are reviewed.
Angioplasty, Balloon ; Balloon Occlusion ; Catheters ; Humans ; Infarction ; Ischemia ; Mortality ; Myocardial Infarction ; No-Reflow Phenomenon ; Thrombosis

Profound reduction of anterograde coronary flow with concomitant ischemia is seen occasionally during percutaneous coronary intervention despite technically successful procedure. We found interesting coronary flow pattern in a patient with acute myocardial infarction, showing angiographic no reflow phenomenon after direct PTCA. The coronary blood flow pattern of the angiographic no-reflow phenomenon in this case was characterized by minimal systolic flow and sharp deceleration of diastolic flow. Coronary flow reserve calculated by the ratio of adenosine induced maximal hyperemic velocity and basal velocity was reduced. The Dopplertipped guide wire was useful for observation of phasic coronary flow pattern of angiographic no-reflow phenomenon.
Adenosine ; Deceleration ; Humans ; Ischemia ; Myocardial Infarction* ; No-Reflow Phenomenon ; Percutaneous Coronary Intervention

No abstract available.
Ischemia*

No abstract available.
Ischemia*

No abstract available.
Ischemia

Recently, percutaneous coronary intervention has been the treatment of choice in most acute myocardial infarction cases. Although the results of percutaneous coronary interventions have ben good, the no-reflow phenomenon and distal embolization of intracoronary thrombus are still major problems even after successful interventions. In this article, we will briefly review the deleterious effects of no-reflow and distal embolization of intracoronary thrombus during percutaneous coronary interventions. The current trials focused on the prevention and treatment of the no-reflow phenomenon and intracoronary thrombus.
Myocardial Infarction ; No-Reflow Phenomenon ; Percutaneous Coronary Intervention ; Thrombosis

If in the aneurysmal rupture patients the brain metabolic parameters obtained from blood chemistry were significant and useful in clinical practice, it cannot be overstimated. Hansdorfer er al.(1973) reported that lactate, pyruvate, uric acid and alpha-HBDH of central venous blood obtained form the patients with brain contusion in basal metabolic state were significantly increased and they were useful in evaluating the prognosis of the patients. Zooping(1970) and Broderson(1974) also had tried to evaluate the prognosis and brain metabolic status of the comatous patients with blood gas analysis and CSF biochemistry. They encouraged us to estimate lactate and lactate/pyruvate ratios of canine jugular venous blood combined with gas analysis. Complete cerebral bloody-ischemia similar with initial stage of aneurysmal rupture was induced by the instanteneous elevation of intracranial pressure 30 mmHg above systemic arterial pressure by infusion of blood and mock CSF mixture into the cisterna arrest or pulmonary hypertension were discarded. At the end of the 5 minutes ischemic period, the needle tip which was inserted in to cisterna magna was removed without decreasing intracranial pressure. At 3 hours, 24 hours, 48 hours and 72 hours after ischemic period jugular venous and arterial blood were sampled for determination of lactate and pyruvate, and blood gas analysis. The following results were obtained. ie ; 1. Both lactate and pyruvate of canine jugular venous blood were increased from 3 hours and reached peak level at 24 hours after insult. Standard value of lactate and pyruvate were 1.416mM and 0.075mM and peak values were 2.429 and 0.165mM(P<0.05). 2. The more severe the neurological deficits of the animals, the highest levels of lactate and pyruvate were observed. 3. The lactate concentrations in 48 hours and 72 hours sample slopped down from 24 hours peak level but were significantly higher than those of standard. 4. Pyruvate returned to the normal range within 48 hours after insult. 5. L/P ratios were not changed significantly until 48 hours after insult but steeply elevated in 72 hours sample. 6. In gas analysis all the animals show respiratory alkalosis after insult. 7. In arterial boundary zones multiple focal ischemia were found in necropsy which was thought as reflecting no-reflow phenomenon. We concluded that elevation of lactate and pyruvate in early stage must be due to the hyperventilation after insult and lactate of late stage reflected CSF lactic acidosis.
Acidosis, Lactic ; Alkalosis, Respiratory ; Aneurysm ; Animals ; Arterial Pressure ; Biochemistry ; Blood Gas Analysis ; Brain ; Brain Injuries ; Chemistry ; Cisterna Magna ; Humans ; Hypertension, Pulmonary ; Hyperventilation ; Intracranial Pressure ; Ischemia ; Lactic Acid* ; Needles ; No-Reflow Phenomenon ; Prognosis ; Pyruvic Acid ; Reference Values ; Rupture ; Uric Acid

BACKGROUND: Successful resuscitation of the brain requires unimpaired blood recirculation. However, unfortunately there are several factors against the successful recirculation. No-reflow phenomenon, characterized by a lack of reperfusion after cerebral ischemia, is the most important pathogenic factor during the early period of spontaneous circulation(ROSC). This study addresses question that pentoxifylline(PTX) ameliorates no-reflow phenomenon after cardiac arrest. METHODS: Fourteen rats were divided three group ; Sham group(n=2), 12 minutes cardiac arrest group without PTX(group I, n=6), and 12 minutes cardiac arrest group pretreated with PTX(group II, n=6). Group II were premedicated by intravascular injection of 5mg/kg PTX into the external jugular vein before 5minutes of the arrest-induction. We induced cardiac arrest with endotracheal clamping and muscle relaxant. And then, resuscitation was initiated. Arterial blood samples were drawn at the femoral artery before 5 minutes of arrest-induction and at the 5 minutes after restoration of ROSC. Reperfusion of brain was visualized by injection of 0.3g/kg of 15% FITC-albumin at 5 minutes after restoration of ROSC, and the animals were decapitated 2 minutes later. The left hemisphere was fixed with 4% formalin, and coronal sections of 200um thickness at three different standard levels of the rat brain were investigated with fluorescence microscopy. Density of microvasular filling were identified and calculated. RESULTS: Our observation demonstrated that 1. There were no significant differences of blood pressures, heart rates, and results of blood gas analysis between group I and II during the prearrest steady state. 2. There were no significant differences of blood pressures, heart rates, and results of blood gas analysis between group Iand II at 5minutes after ROSC. 3. Group II premedicated with PTX, showed significant increased capillary refiling(0.310+/-0.035)than group I without PTX(0.181+/-0.040). CONCLUSIONS : The results showed that during the prearrest steady state, premedication of PTX ameliorated the no-reflow phenomenon in the rat model of the asphyxial arrest. Further experimental studies are required to focus on the effects of postarrest infused PTX, The neurologic outcome, and the clinical applications.
Animals ; Blood Gas Analysis ; Brain ; Brain Ischemia ; Capillaries ; Constriction ; Femoral Artery ; Formaldehyde ; Heart Arrest* ; Heart Arrest, Induced ; Heart Rate ; Jugular Veins ; Microscopy, Fluorescence ; Models, Animal ; No-Reflow Phenomenon* ; Pentoxifylline* ; Premedication ; Rats* ; Reperfusion ; Resuscitation

The object of this investigation was to study the effects of mannitol and high dose of methylprednisolone(MP)upon evolution of cerebral infarction in cats after acute left middle cerebral artery(MCA) occlusion and following reperfusion. The acute occlusion of left proximal MCA of thirty cats for 2, 4 and 6 hours respectively were accomplished by applying the Heifetz clip through the retroorbital extradural approach and followed by 2 hours of recirculation. Fifteen cats were untreated as a control group and the fifteen cats were given a combination of mannitol(2g/kg) and MP (15mg/kg) at 30 minutes after occlusion initially, and then every one and a half hour. Results of morphologic examination of the brain demonstrated that untreated cats undergoing 2-hour or 4-hour occlusion mannitol and MP improved the ischemic edema and infarction, but in treated cats undergoing 6-hour occlusion they had little protective effect in ischemic brain injury(swelling, neuronal damage and hemorrhagic infarction). Electronecephalography(EEG) in cats undergoing 2-or 4-hour occlusion showed more increasing activities and voltage than in untreated groups, but in cats undergoing 6-hour occlusion low. voltage and slow waves with poor activity, i.e, generally suppressed pattern, were observed and were not significantly different between treated and untreated groups. Our experimental studies of the therapeutic beneficial effects of mannitol and MP were observed in cats of 2-or 4-hour occlusion of MCA with 2 hour recirculation. Therefore, it was suggested that mannitol and MP will prolong the period of potential reversibility of cerebral ischemia following reperfusion within 4 hours of ischemia.
Animals ; Brain ; Brain Ischemia ; Cats ; Cerebral Infarction* ; Edema ; Infarction ; Ischemia ; Mannitol* ; Methylprednisolone* ; Neurons ; Reperfusion