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J N Graziano

Publications and source records attributed to J N Graziano.

8 recordsLinked to original sources
PubMed2002

The influence of a restrictive atrial septal defect on pulmonary vascular morphology in patients with hypoplastic left heart syndrome.

Hypoplastic left heart syndrome (HLHS) with a restrictive atrial septal defect (ASD) is a form of congenital heart disease with considerable morbidity and mortality. This morphologic analysis assesses the pulmonary vasculature in this patient population. Pulmonary arteries, the persistence of high-resistance fetal arterioles, pulmonary veins, and lymphatics from multiple lung sections from each of five patients with HLHS and a restrictive ASD were compared to those of five patients with HLHS and nonrestrictive ASD. Lung sections from each patient were qualitatively graded in severity of pathology from 0 to 3 for each of the structures described previously, with the pathologist blinded to the status of the ASD. Patients with a restrictive ASD exhibited more significant pulmonary venous thickening and lymphatic dilatation (p = 0.02), with a tendency toward persistence of high-resistance fetal vessels (p = 0.2), compared to patients with a nonrestrictive ASD. These findings imply that patients with HLHS and a restrictive ASD possess pulmonary vascular abnormalities that place them at higher risk for the current surgical interventions available compared to patients with a nonrestrictive ASD.

Female↗
PubMed1993

Multiple modes of termination of re-entrant excitation around an anatomic barrier in the canine atrium during the action of d-sotalol.

In the chronically-instrumented animal and the isolated blood perfused heart, atrial re-entry via a fixed path around an anatomic obstacle has been described and is terminated by the class III antiarrhythmic agent d-sotalol. The precise mechanism by which d-sotalol terminates this arrhythmia is not known. In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart (n = 5) during episodes of sustained flutter and drug administration were determined. A fixed array of bipolar electrodes was used to record endocardial electrograms from 96 sites on the RA simultaneously. Maps of all control flutters showed that the rhythm was due to persistent circus movement of the impulse around the tricuspid valve ring. d-Sotalol was effective in terminating atrial re-entry in this model. In all episodes, block of the excitatory impulse in a specific region of the re-entrant circuit accompanied these terminations. However, the events preceding the occurrence of block of the impulse were not similar. Two different modes of termination are described. The class III antiarrhythmic agent d-sotalol can terminate atrial re-entry in several ways. In one mode, complete conduction block of the re-entering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original re-entrant circuit occurs when there is failure of a lateral boundary. In both modes cycle length (CL) oscillations are observed.

Animals↗
PubMed1993

Activation mapping of reentry around an anatomical barrier in the canine atrium: observations during the action of the class III agent, d-sotalol.

INTRODUCTION: In the chronically instrumented animal and the isolated blood perfused heart, atrial reentry via a fixed path around an anatomical obstacle has been described and is terminated by the Class III antiarrhythmic agent, d-sotalol. The precise mechanism by which d-sotalol terminates this arrhythmia is not known. METHODS AND RESULTS: In the present study, right atrial (RA) activation sequences in the isolated, coronary artery perfused canine heart during episodes of sustained flutter (n = 7) and drug administration were determined. A fixed array of bipolar electrodes was used to record endocardial electrograms from 96 sites on the RA simultaneously. Maps of all control flutters showed that the rhythm was due to persistent circus movement of the impulse around the tricuspid valve ring. D-sotalol was effective in terminating atrial reentry in this model. In all episodes, block of the excitatory impulse in a specific region of the reentrant circuit accompanied these terminations. However, the events preceding the occurrence of block of the impulse were not similar. Two different modes of termination are described. CONCLUSION: The Class III antiarrhythmic agent d-sotalol can terminate atrial reentry in several ways. In one mode, complete conduction block of the reentering impulse within the fixed path occurs to terminate the rhythm. In the other mode, interruption of the original reentrant circuit occurs when there is failure of a lateral boundary. Often in this latter case, interruption of the original circuit is by an extra impulse that is secondary to a change in the path of the impulse. In both modes cycle length oscillations are observed.

Animals↗
PubMed1993

Endocardial mapping of reentry around an anatomical barrier in the canine right atrium: observations during the action of the Class IC agent, flecainide.

INTRODUCTION: Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y-shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier. METHODS AND RESULTS: To investigate the mechanism of flecainide-induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 +/- 24 msec) by 89% to 309 +/- 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In five episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (+/- 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long-short cycle length oscillations led to return reexcitation by the impulse within the primary path and subsequent termination. CONCLUSION: In summary, similar to our previous findings with the Class III agent, d-sotalol, two different modes of termination of atrial reentry were observed with flecainide.

Animals↗
PubMed1991

Intravenous anti-D treatment of immune thrombocytopenic purpura: analysis of efficacy, toxicity, and mechanism of effect.

The efficacy, toxicity, and mechanism of effect of intravenous Anti-D (Winrho) were studied in 43 Rh+ patients with immune thrombocytopenia purpura (ITP) who had not undergone splenectomy and in three already splenectomized patients. The mean platelet increase for the 43 nonsplenectomized patients was 95,000/microL (median 43,000/microL). Children had greater acute platelet responses than did adults. Human immunodeficiency virus status and duration of thrombocytopenia did not affect response. Maintenance treatment was given to patients as needed: the average interval between infusions was 24 days. The three splenectomized patients had no platelet response whatsoever. Toxicity was minimal; infusions were completed in less than 5 minutes. The generally accepted mechanism of effect of Anti-D has been Fc receptor blockade by substitution of antibody-coated red blood cells for antibody-coated platelets. Evidence is presented suggesting that the effect of IV Anti-D is not limited to Fc receptor blockade, including: (1) no correlation of parameters of hemolysis with platelet increase; (2) a 48- to 72-hour delay before platelet increase; (3) a tendency of the change in monocyte Fc receptor I expression to correlate with platelet increase; and (4) increased in vitro production of antibodies to sheep red blood cells following IV Anti-D infusion.

Adult↗
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Heart Septal Defects, Atrial↗
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Thrombosis in the intensive care unit: etiology, diagnosis, management, and prevention in adults and children.

Venous thromboembolism, a well-recognized complication in postoperative patients, is emerging as a frequent complication in critically ill patients in intensive care units. Diagnosis can be particularly difficult in such patients because underlying systemic illnesses may mask common presenting signs and symptoms. Although numerous independent risk factors have been identified, the critical role of both central venous catheters and prothrombotic disorders as significant risk factors is a common theme in the pediatric and adult literature. Various diagnostic tests exist, with venography remaining the gold standard and newer, less invasive methods such as ultrasonography and impedance plethysmography becoming increasingly popular. Standard unfractionated heparin remains the mainstay of therapy and prophylaxis, although the use of low molecular weight heparins is becoming more commonplace. Thrombolytic therapy continues to be reserved for severe, life-threatening, acute thrombosis. In this article, we review the common risk factors, diagnostic modalities, and treatment options for venous thromboembolism in critically ill adult and pediatric patients.

Adult↗