Incidental detection of an intracardiac cement embolism complicating percutaneous vertebroplasty during cardiac catheterization: A case report.

Percutaneous vertebroplasty has emerged as an increasingly popular intervention for managing a variety of common spinal conditions. Nevertheless, kyphoplasty cement can accidentally leak into paravertebral venous plexus, then travel to the right heart chambers through the venous system. We report an exceedingly rare case of an intracardiac cement embolism, likely an inadvertent complication of a recent percutaneous lumbar vertebroplasty. A mobile mass was incidentally found during a cardiac catheterization procedure, most likely in right atrium. Subsequent computed tomography angio chest and cardiac imaging confirmed a floating foreign body in the right atrium, which was then retrieved successfully through an endovascular approach. Gross examination of the removed body confirmed a bone cement-like material. Intracardiac cement embolism warrants serious attention as it may result in catastrophic cardiac complications. Learning objective: Intracardiac cement embolism is an extremely rare, but potentially life-threatening complication after percutaneous vertebroplasty. The bone cement fragments accidentally leak into paravertebral plexus and then via venous system into the right-sided cardiac chambers and pulmonary arteries.

Potential contribution of open-cell stent design to balloon entrapment and review of techniques to recover.

Balloon entrapment during coronary angioplasty is a rare but potentially disastrous complication of percutaneous coronary intervention (PCI), described during both angioplasty alone, as well as with stents. This report describes the case of an entrapped stent-balloon within an extremely calcified proximal left anterior descending artery (LAD) lesion, and reviews techniques and strategies that can be applied in similar situations. In this case, we suspect the open-cell design of the specific stent used, combined with the high radial force of the calcified lesion, led to a "pincer effect," and entanglement of the balloon material within the stent scaffolding. After exhaustion of all percutaneous options to retrieve the balloon, the patient was ultimately taken for urgent cardiac surgery for extraction of the balloon and vein patch of the LAD.

Evaluating the optimal activated clotting time during carotid artery stenting.

Carotid artery stenting is an alternative to carotid endarterectomy for patients at high risk for surgery for carotid artery stenosis. Although unfractionated heparin is routinely used, there are no published data evaluating the optimal activated clotting time during carotid stenting. In a retrospective analysis of 605 patients who underwent carotid stenting using unfractionated heparin at the Cleveland Clinic Foundation, the optimal peak procedural activated clotting time associated with the lowest combined incidence of death, stroke, or myocardial infarction was 250 to 299 seconds.

The duration of hypotension before the initiation of antibiotic treatment is a critical determinant of survival in a murine model of Escherichia coli septic shock: association with serum lactate and inflammatory cytokine levels.

BACKGROUND: This study was designed to examine the relationship between the timing of antibiotic treatment and both survival rates and hemodynamic/inflammatory correlates of survival in a murine model of Escherichia coli septic shock. METHODS: Surgical implantation of an E. coli (O18:K1:H7)-laced, gelatin capsule-encased fibrinogen clot was used to generate a bacteremic model of murine septic shock. Survival duration, hemodynamic responses, and circulating serum tumor necrosis factor (TNF)-alpha , interleukin (IL)-6, and lactate levels were assessed in relation to increasing delays in or absence of antibiotic treatment. RESULTS: A critical inflection point with respect to survival occurred between 12 and 15 h after implantation. When initiated at or before 12 h, antibiotic treatment resulted in < or = 20% mortality, but, when initiated at or after 15 h, it resulted in >85% mortality. Physiologically relevant hypotension developed in untreated septic mice by 12 h after implantation. Values for heart rate differed between untreated septic mice and sham-infected control mice by 6 h after implantation, whereas values for cardiac output and stroke volume did not differ until at least 18-24 h after implantation. Antibiotic treatment initiated > or = 12 h after implantation was associated with persistence of increased circulating serum lactate, TNF- alpha , and IL-6 levels. CONCLUSIONS: The timing of antibiotic treatment relative to hypotension is closely associated with survival in this murine model of septic shock. Delay in antibiotic treatment results in the persistence of inflammatory/stress markers even after antibiotic treatment is initiated.

Drug-eluting stents: the beginning of the end of restenosis?

In multiple clinical trials, patients who received drug-eluting stents instead of plain stents during percutaneous coronary interventions had rates of restenosis that were lower by roughly one half to three fourths, depending on how restenosis was defined and on the population studied. These stents will likely be used more and more as their indications evolve.

Preload-independent mechanisms contribute to increased stroke volume following large volume saline infusion in normal volunteers: a prospective interventional study.

INTRODUCTION: Resuscitation with saline is a standard initial response to hypotension or shock of almost any cause. Saline resuscitation is thought to generate an increase in cardiac output through a preload-dependent (increased end-diastolic volume) augmentation of stroke volume. We sought to confirm this to be the mechanism by which high-volume saline administration (comparable to that used in resuscitation of shock) results in improved cardiac output in normal healthy volunteers. METHODS: Using a standardized protocol, 24 healthy male (group 1) and 12 healthy mixed sex (group 2) volunteers were infused with 3 l normal (0.9%) saline over 3 hours in a prospective interventional study. Individuals were studied at baseline and following volume infusion using volumetric echocardiography (group 1) or a combination of pulmonary artery catheterization and radionuclide cineangiography (group 2). RESULTS: Saline infusion resulted in minor effects on heart rate and arterial pressures. Stroke volume index increased significantly (by approximately 15-25%; P < 0.0001). Biventricular end-diastolic volumes were only inconsistently increased, whereas end-systolic volumes decreased almost uniformly. Decreased end-systolic volume contributed as much as 40-90% to the stroke volume index response. Indices of ventricular contractility including ejection fraction, ventricular stroke work and peak systolic pressure/end-systolic volume index ratio all increased significantly (minimum P < 0.01). CONCLUSION: The increase in stroke volume associated with high-volume saline infusion into normal individuals is not only mediated by an increase in end-diastolic volume, as standard teaching suggests, but also involves a consistent and substantial decrease in end-systolic volumes and increases in basic indices of cardiac contractility. This phenomenon may be consistent with either an increase in biventricular contractility or a decrease in afterload.