Developmental dysplasia of the hip and ultrasound. More is less?
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Hip Dislocation, Congenital↗
Biomedical subjects
R Hernandez
Publications and source records attributed to R Hernandez.
Findings of coronary angioscopy in angiographically normal coronary segments of patients with coronary artery disease.
Compared with pathologic studies coronary angiography is a relatively insensitive technique to detect early atherosclerosis. Coronary angioscopy is a new technique providing direct information on luminal vessel surface. To determine whether coronary angioscopy may detect the presence of atherosclerotic disease on angiographically normal coronary segments, 52 patients underwent a study with coronary angioscopy before coronary angioplasty. The mean age was 59 +/- 10 years; 46 patients were men and 6 were women. The reason for coronary angioplasty was unstable angina in 36 patients, stable angina in 8 patients, and silent ischemia in 8 patients. In seven patients angiography revealed luminal irregularities on the coronary segment proximal to the culprit lesion, and all these patients also had proximal disease as demonstrated by coronary angioscopy. In the remaining 45 (87%) patients angiography revealed a smooth-vessel contour proximal to the target lesion. On quantitative angiography these "normal" coronary segments measured 2.8 +/- 0.4 mm in luminal diameter. In 30 (67%) of these patients angioscopy revealed proximal disease on the vessel wall, but in 15 (33%) patients the luminal surface of these segments also appeared normal on angioscopy. Disease as detected by angioscopy in angiographically normal segments included yellow plaque in 19 patients, mural thrombus in 5, mixed plaques in 4, and small flaps in 2 patients. In eight patients coronary angioscopy detected that atherosclerotic disease extended proximally from the target lesion, but in the remaining 22 patients the angioscopic findings appeared to be discrete and well separated from the angiographic lesion. All these plaques were relatively small and did not protrude into the coronary lumen.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Angioscopic findings during coronary angioplasty of coronary occlusions.
OBJECTIVES: This study sought to elucidate angioscopic findings in totally occluded vessels before and after intervention. BACKGROUND: Coronary angioscopy allows direct visualization of the lumen surface of the coronary arteries; however, the utility of coronary angioscopy during coronary angioplasty of vessels with a total occlusion is unknown. METHODS: Twenty-one consecutive patients (mean [+/- SD] 58 +/- 9 years, range 39 to 77; 3 women, 18 men) undergoing dilation of an occluded vessel were studied with coronary angioscopy. Occlusions were classified as functional in 8 patients (Thrombolysis in Myocardial Infarction [TIMI] flow grade 1) and anatomic in 13 (TIMI flow grade 0). Once the guide wire had crossed the occlusion, coronary angioscopy was attempted before and after angioplasty. RESULTS: In all patients, coronary angioscopy before dilation visualized protruding material occluding the coronary lumen where the guide wire was wedged. The occlusion consisted of red thrombus in 19 patients (90%) (2 with isolated occlusive thrombus, 17 with thrombus associated with atherosclerotic plaque) and protruding yellow plaque in 2 patients (10%). However, on angiography only 7 occlusions (33%) had data consistent with thrombus (p < 0.01 vs. coronary angioscopy). Successful dilation was obtained in 20 patients. After dilation, coronary angioscopy was repeated in 18 patients, revealing residual thrombus with plaque in 16 (89%) and a residual yellow plaque in 2. In addition, coronary angioscopy revealed coronary dissections in 13 patients (72%); however, angiography revealed dissections only in 10 patients (55%) and residual thrombus in 2 (10%) (p < 0.001). In one patient, coronary angioscopy visualized silent distal embolization of a red thrombus not previously recognized on angiography. CONCLUSIONS: Before intervention, coronary angioscopy provides unique insights into the pathologic substrate of occluded coronary vessels. An occlusive plaque with thrombus is the most common underlying substrate in these lesions. After successful dilation, angiographically silent mural thrombus is seen in most patients. This information could be used to assist in the selection of candidates and type of coronary interventions and could also prove to be of prognostic value in patients with occluded vessels.
Angioplasty, Balloon, Coronary↗
Differential effects of acute thermal injury on rat splanchnic and renal blood flow and prostanoid release.
This study examines the hypothesis that acute thermal injury decreases renal and splanchnic blood flow which correlates with altered endogenous vasodilator eicosanoid release. Anesthetized male Wistar rats were subjected to sham or a non-resuscitated 30% total body surface area burn. At 1, 2, 4, 8, and 24 h post-burn mean arterial pressure as well as superior mesenteric and renal artery in vivo blood flow were measured. The superior mesenteric and renal arteries were cannulated and perfused in vitro with their end organs with Krebs buffer (pH 7.4, 37 degrees C). Renal and splanchnic 6-keto-PGF1 alpha (PGI2), PGE2, and thromboxane B2 (TXB2) release were measured by EIA at 15 min of perfusion. Renal and superior mesenteric artery blood flow decreased by 40% or more at 1 and 2 h post-burn despite mean arterial pressure remaining unchanged. The major eicosanoids released were PGI2 from the splanchnic bed and PGI2 and PGE2 from the kidney. Splanchnic PGI2 and TXB2 release and renal TXB2 increased 2-3 fold at 1 h post-burn but returned to the sham level at 2 h post-burn. By 24 h post-burn the vasodilator eicosanoids were increased in both the splanchnic and renal vascular beds. These data show that decreased renal and splanchnic blood flow was associated with increased endogenous release of the potent vasoconstrictor TXB2. By 2 h post-burn, renal and splanchnic blood flow began returning toward the sham level as endogenous release of TXB2 from both organs fell to sham levels. These data suggest that increased endogenous release of TXB2 may contribute to the short-term decrease in renal and splanchnic blood flow in the immediate post-burn period and thus may contribute to ischemia of both vascular beds.
6-Ketoprostaglandin F1 alpha↗
Acute burn down regulates rabbit splanchnic and renal prostanoid release.
This study examines the hypothesis that acute thermal injury decreases renal and splanchnic vasodilator eicosanoids. Anesthetized rabbits were subjected to sham or a 25% total body surface area burn and fluid resuscitated. At 2, 4, 6, 12, and 24 h postburn the superior mesenteric and renal arteries were cannulated and perfused in vitro with their end organs with Krebs buffer (pH 7.4, 37 degrees C). Renal and splanchnic prostaglandins (PGs) 6-keto-PGF1 alpha (PGI2), and PGE2, and thromboxane B2 (TxB2) release were measured by EIA at 15 min of perfusion. The major eicosanoids released were PGI2 from the splanchnic bed and PGI2 and PGE2 from the kidney. Renal PGE2 and PGI2 and splanchnic PGI2 release were decreased by 50% or more 12 h postburn (p < 0.01) but were restored to sham burn levels 24 h postburn. Loss of these endogenous renal and splanchnic vasodilators 12 h postburn may contribute to ischemia of both vascular beds at this critical time period following acute burn injury.
6-Ketoprostaglandin F1 alpha↗
Oxygen free radicals regulate splanchnic nitric oxide synthesis and blood flow.
This study examines the hypothesis that oxygen radicals down-regulate splanchnic nitric oxide synthesis and contribute to splanchnic vasoconstriction following hemorrhage/reperfusion injury. Anesthetized rats underwent placement of flow probes around the superior mesenteric artery and abdominal aorta. Animals were bled to 30 mmHg for 30 min, reperfused without or with superoxide dismutase, an oxygen radical scavenger, 15 min before reperfusion and compared with sham-treated rats. Animals were sequentially treated with the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) at 10 mg/kg and L-arginine, a nitric oxide precursor, at 200 mg/kg or 400 mg/kg. L-NAME increased systemic pressure and decreased superior mesenteric artery blood flow whereas L-arginine decreased arterial pressure and increased superior mesenteric artery blood flow in the sham animals. Hemorrhage/reperfusion injury attenuated the pressure and superior mesenteric artery blood flow changes following L-NAME and L-arginine dosing, which was reversed by superoxide dismutase treatment. These data suggest that oxygen free radicals regulate splanchnic nitric oxide synthesis, thus contributing to splanchnic vasoconstriction following hemorrhage/reperfusion injury.
Animals↗
Possible role for oxygen free radicals in the regulation of renal nitric oxide synthesis and blood flow.
BACKGROUND: This study examines the hypothesis that oxygen radicals down-regulate renal nitric oxide synthesis and contribute to renal vasoconstriction after hemorrhage/reperfusion injury. METHODS: Arterial pressure and renal artery blood flow were measured in anesthetized rats subjected to sham or hemorrhage (30 mm Hg for 30 minutes) followed by blood reperfusion without or with superoxide dismutase, an oxygen radical scavenger. Animals were sequentially injected with 10 mg/kg NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, and 200 mg/kg and 400 mg/kg L-arginine, a nitric oxide precursor. RESULTS: The L-NAME treatment increased arterial pressure and decreased renal artery blood flow whereas L-arginine decreased arterial pressure and decreased renal blood flow in the sham animals. Hemorrhage/reperfusion injury attenuated the pressure and renal blood flow changes following L-NAME and L-arginine treatment, which was reversed by superoxide dismutase. CONCLUSIONS: These data suggest that oxygen radicals contribute to the regulation of renal nitric oxide synthesis, contributing to renal artery vasoconstriction following hemorrhage/reperfusion injury.
Analysis of Variance↗
Usefulness of the codification of multiple causes of death in mortality statistics.
BACKGROUND: The codification of multiple causes of death began in the US in 1917 and systematic publication of this data started in 1984. In Spain this began in 1988, and the data from this year have been taken as the basis for investigation. They have also been studied for regional differences. METHODS: A representative sample (595) of Spanish Standard Death Certificates (DC) was collected in Asturias for the year 1988. All were coded according to the International Classification of Diseases and a separate coding was made for each nosological entity included in the certificate (coding of multiple causes). The median, mode and the multiple cause/underlying cause ratio were also calculated. RESULTS: More than 80% of the certificates studied contained more than one cause of death. Chronic diseases are those which are accompanied by a greater number of causes and acute diseases those which appear alone. The highest ratios appear for diseases which are ill defined and also in those which are chronic. CONCLUSIONS: Our data show that information is lost in the production of the statistics of mortality and there are repercussions for the usefulness of these statistics.
Cause of Death↗
Neutrophil regulation of splanchnic blood flow after hemorrhagic shock.
OBJECTIVE: This study examines the hypothesis that neutrophils impair splanchnic blood flow during resuscitation from hemorrhage by inhibiting the release of the compensatory vasodilator PGI2 from the bowel. SUMMARY BACKGROUND DATA: Resuscitation from hemorrhagic shock is associated with neutrophil infiltration into the intestine, reduced splanchnic perfusion, and reduced release of PGI2 from the intestine. METHODS: Sprague-Dawley rats received either vinblastine (VIN) to deplete circulating neutrophils or normal saline (NS). These animals then underwent either hemorrhage and resuscitation (SK + R) or sham operation (SHAM). Superior mesenteric artery flow and splanchnic 6-keto PGF1a (metabolite of PGI2) release were measured. RESULTS: Superior mesenteric artery blood flow was significantly greater in VIN-treated animals sustaining SK + R than in those treated with NS (p < 0.05). Neutrophil depletion preserved 6-keto PGF1a release after SK + R, whereas 6-keto PGF1a release in the NS-treated, SK + R group was significantly reduced (p < 0.05). CONCLUSION: These data are compatible with the hypothesis that neutrophils may influence splanchnic perfusion after SK + R by inhibiting splanchnic PGI2 release.
Animals↗
Peritoneal migration of an abdominally implanted epicardial pacemaker: a cause of intestinal obstruction.
We report the case of a 10-year-old child with an abdominally implanted epicardial pacemaker that eroded through the peritoneum and migrated to an intraperitoneal location, resulting in partial and then complete intestinal obstruction. This potentially life-threatening complication should be considered when a patient with an abdominally implanted pacemaker presents with abdominal pain.
Child↗
Lyme disease: debilitating, yet preventable.
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Animals↗
Induction of acute hypocalcemia in rats.
Decreased plasma calcium levels could produce important changes in cellular functions and drug responses. This communication describes the temporal decrease in calcemia that can be obtained in Sprague-Dawley rats after the ip administration of doses of 1 to 16 IU calcitonin. The injections caused significant reductions in calcemia in this strain of rats, but did not alter the behavior or general condition of the dosed animals. The method described permits the establishment of experimental models of hypocalcemic rats that will be very useful for physiological and pharmacological studies.
Animals↗
Resuscitation of ischemia/reperfusion with hyperalimentation increases intestinal PGI2 synthase (PS) content and PGI2 release.
Normal rat splanchnic blood flow and eicosanoid synthesis were compared to sham (Sham) and hemorrhage/reperfusion (SK + R) animals treated with 5 days of total parenteral nutrition (TPN). After in vivo measurement of superior mesenteric artery (SMA) blood flow, the splanchnic bed was perfused in vitro and venous effluent assayed for eicosanoid release by EIA. Aortic, SMA, ileal muscularis/serosa, and mucosa homogenates were analyzed for cyclooxygenase (COX) and prostacyclin synthase (PS) content by Western blot and for COX activity by radiochromatography. SK + R + TPN decreased SMA blood flow 33% and increased splanchnic PGI2 release twofold (p < .05) compared with the Sham +TPN and normal groups. groups SK + R + TPN did not alter COX activity in any of the tissues but Western blot analysis showed a twofold increase in COX and PS content in ileum muscularis/serosa (p < .05). These data show that SK + R + TPN induced a decrease in SMA blood flow and a compensatory increase in release of splanchnic PGI2. The mechanism for increased splanchnic PGI2 release after SK + R + TPN was an increase in PS and COX content (not activity) in the ileal muscularis/serosa.
Animals↗
Angiographic deterioration of the previously dilated coronary segment induced by angioscopic examination.
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Adult↗
Determinants of coronary compliance in patients with coronary artery disease: an intravascular ultrasound study.
OBJECTIVES: The aim of this study was to elucidate determinants of coronary compliance in patients with coronary artery disease. BACKGROUND: Intravascular ultrasound potentially enables in vivo evaluation of coronary artery compliance. METHODS: Twenty-seven patients (mean age [+/- SD] 57 +/- 11 years, three women) undergoing coronary angioplasty were studied with intravascular ultrasound imaging. A mechanical intravascular ultrasound system (4.8F, 20 MHz) was used. A total of 58 different coronary segments (proximal to the target angiographic lesion) were studied. Of these, 35 were located in the left anterior descending, 9 in the left main, 8 in the left circumflex and 6 in the right coronary arteries. During intravascular ultrasound imaging, 22 segments (38%) appeared normal, but 36 (62%) had plaque (24 fibrotic, 3 lipidic and 9 calcified). Systolic-diastolic changes in area (delta A) and pressure (delta P) with respect to vessel area (A) were used to study normalized compliance (Normalized compliance = [delta A/A]/delta P [mm Hg-1 x 10(3)]). RESULTS: Lumen area and plaque area were 12.6 +/- 5.7 and 3 +/- 3 min2, respectively. Plaque was concentric (more than two quadrants) at 10 sites, but the remaining 26 plaques were eccentric. Compliance was inversely related to age (r = -0.34, p < 0.05) but was not related to other clinical variables. Compliance was greater in the left main coronary artery (3.9 +/- 2.1 vs. 1.8 +/- 1.2 mm Hg-1, p < 0.05) and in coronary segments with normal findings on ultrasound imaging (2.9 +/- 1.9 vs. 1.6 +/- 1.1 mm Hg-1, p < 0.01). Moreover, at diseased coronary segments compliance was lower in calcified plaques than in other types of plaques (1.2 +/- 0.7 vs. 2.3 +/- 1.6 mm Hg-1, p < 0.01) but was similar in concentric and eccentric plaques (1.6 +/- 1.5 vs. 1.6 +/- 0.9 mm Hg-1). Plaque area (r = -0.38, p < 0.01) was inversely correlated with compliance. On multivariate analysis, only age and plaque area were independently related to compliance. CONCLUSIONS: Intravascular ultrasound may be used to evaluate compliance in patients with coronary artery disease. Compliance is reduced with increasing age and is mainly determined by the arterial site and by the presence, size and characteristics of plaque on intravascular ultrasound imaging.
Age Factors↗
Early angiographic changes of side branches arising from a Palmaz-Schatz stented coronary segment: results and clinical implications.
OBJECTIVES: The purpose of this study was to assess the effects and clinical implications of Palmaz-Schatz stent implantation on coronary blood flow in side branches arising from a stented coronary artery segment. BACKGROUND: The occlusion of a side branch is a well defined risk after balloon angioplasty. However, the impact of stenting on the coronary flow in side branches arising within the stented segment is unknown. METHODS: Forty-six stented coronary artery segments with 79 side branches emerging from the stented segment were analyzed. Angiographic studies were performed before angioplasty, after balloon dilation, immediately after stenting and 24 h later. Side branches were classified as follows: type A (> or = 1 mm in diameter, with ostial narrowing), type B (> or = 1 mm in diameter, without ostial narrowing), type C (< 1 mm in diameter, with ostial narrowing) and type D (< 1 mm in diameter, without ostial narrowing). Quantitative angiography was used to assess the diameter of the side branches. RESULTS: Stents were implanted electively in lesions with restenosis (41 stents, 89%) or with a suboptimal result after angioplasty (5 stents, 11%). Nine side branches (11%) were type A, 25 (32%) type B, 7 (9%) type C and 38 (48%) type D. At baseline, 68 side branches had Thrombolysis in Myocardial Infarction (TIMI) trial flow grade 3; 10 had grade 2; and 1 had grade 1. Flow worsened (TIMI grade > or = 1) in six side branches (8%) after balloon dilation and in four side branches (5%) after stenting. One additional side branch (1%) was occluded at 24 h. Of the 34 side branches > or = 1 mm in diameter (mean diameter 1.5 +/- 0.3 mm), 2 (6%) had flow impairment after stenting. Three patients experienced transient angina, but no acute myocardial infarction occurred as a result of a side branch occlusion. CONCLUSIONS: Coronary artery stenting does not modify anterograde flow in 90% of side branches. Coronary flow is reduced after stenting in a few branches, but this does not appear to have major clinical relevance.
Angioplasty, Balloon, Coronary↗
Invasion and metastasis mechanisms in Entamoeba histolytica and cancer cells. Some common cellular and molecular features.
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Animals↗
Angiographic changes (Dotter effect) produced by intravascular ultrasound imaging before coronary angioplasty.
Intravascular ultrasound (IVUS) imaging of the coronary arteries has recently been introduced for the study of coronary lesions, but the angiographic effects produced by an IVUS examination before coronary angioplasty are unknown. Accordingly, the feasibility of and the potential angiographic changes caused by IVUS study (4.8F catheter) of severe coronary lesions was prospectively studied. Thirty consecutive coronary lesions were analyzed before intervention (29 patients, mean age 61 +/- 9 years, 5 women and 24 men). Before and after IVUS examination, intracoronary nitroglycerin 0.2 mg, was administered and two orthogonal angiographic views obtained. In 17 (57%) lesions the transducer of the IVUS catheter (radiopaque) could be gently advanced for precise location at the lesion site, and in every case the ultrasonic images revealed that the catheter was wedged into the plaque. In the remaining 13 lesions only the catheter tip but not the transducer could be located at the lesion site. Baseline minimal luminal diameter was similar in the crossed lesions and in lesions that prevented complete advancement of the IVUS catheter (0.86 +/- 0.2 vs 0.82 +/- 0.2 mm, difference not significant). Lesion characteristics could not predict the feasibility of the IVUS study. No complications resulted from the IVUS study. Quantitative angiography (automatic edge-detection system) revealed a significant increment in minimal luminal diameter (0.84 +/- 0.2 vs 1.16 +/- 0.3 mm, p < 0.001) and minimal luminal cross-sectional area (0.67 +/- 0.4 vs 1.09 +/- 0.5 mm2, p < 0.01) after passage of the IVUS catheter.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗