Background

Transcranial Doppler (TCD) can detect a right-to-left shunt (RLS) with high sensitivity but has a 5% chance of a false negative study. TCD is usually performed with injection of agitated saline into an arm vein. We compared the sensitivity of TCD performed from the brachial versus femoral veins.

Methods

Patients presenting to the cardiac catheterization laboratory for percutaneous closure of a patent foramen ovale (PFO) were enrolled. Power M-mode Transcranial Doppler (Terumo 150 PMD) was conducted. After injection of a mixture of 8 cc of agitated saline, 0.5 cc of air, and 1 cc of blood into the brachial vein, embolic tracks were counted over the middle cerebral arteries. The degree of RLS was evaluated by TCD at rest, and with Valsalva at 40 mmHg aided by visual feedback with a manometer device. The test was repeated using femoral venous injections.

Results

Sixty five patients were enrolled, mean age 52, 43% male. TCD grades were significantly higher with femoral injections compared to brachial injections at rest (p<0.0001), and with the Valsalva maneuver (p<0.0001). The presence of a RLS was confirmed by intracardiac echocardiography (ICE) during cardiac catheterization in 62 (95.4%) patients.

Conclusion

The sensitivity of TCD for detection of RLS is increased when agitated saline injections are performed through the femoral vein. In patients with a high clinical suspicion for RLS, low TCD grades obtained with traditional brachial venous access should be interpreted with caution. When possible, a repeat study using femoral venous access may be considered.

Background

Reports of stent thrombosis and death in patients who have received drug-eluting stents (DES) have provoked debate regarding their long-term safety. We investigated the specific causes of death in patients receiving DES at an academic tertiary-care center.

Methods

A retrospective analysis of 1,023 consecutive patients who underwent percutaneous coronary intervention (PCI) with DES from 2003 to 2006 at UCLA Medical Center was performed. Dates and cause of death were obtained by reviewing the patient's medical record, contacting the patient's doctor, or accessing the Social Security Death Index and obtaining copies of death certificates at the Los Angeles County Registrar-Recorder/County Clerk office. If the cause of death could not be determined, it was reported "unknown."

Results

At a mean follow up of 2.9 +/- 1.3 years, 96 patients who underwent PCI with DES died during the analysis (9.4% mortality). The mean duration between index PCI and death was 331 +/- 324 days. The cause of death was unknown in 9 patients, thus the analysis was based upon 87 patients. There were similar number of cardiac (n = 44) and non-cardiac deaths (n = 43). The risk of PCI-related death was 1.3% (13/1023), which included 11 patients (1.1%) who died from stent thrombosis. Fourteen patients (1.4%) who presented with myocardial infarction (MI) and underwent PCI died, and 14 patients (1.4%) died from heart failure. Non-cardiac deaths included cancer, infection, respiratory failure and a cerebrovascular event. Age, chronic renal insufficiency, presentation with MI, chronic obstructive pulmonary disease, history of cerebrovascular event, orthotopic heart transplantation and left ventricular ejection fraction were significantly associated with increased mortality.

Conclusions

Cardiac and non-cardiac causes of death contributed similarly to mortality in patients who underwent PCI with DES at a large tertiary care center that manages high-risk patients. Overall PCI-related death and stent thrombosis causing death were low. The majority of deaths occurred in patients after hospital discharge. The majority of patients who died in the hospital presented with acute MI and were in critical condition on presentation.

The role of atherosclerotic calcification in plaque rupture remains controversial. In previous analyses using finite element model analysis, circumferential stress was reduced by the inclusion of a calcium deposit in a representative human anatomical configuration. However, a recent report, also using finite element analysis, suggests that microscopic calcium deposits increase plaque stress. We used mathematical models to predict the effects of rigid and liquid inclusions (modeling a calcium deposit and a lipid necrotic core, respectively) in a distensible material (artery wall) on mechanical failure under uniaxial and biaxial loading in a range of configurations. Without inclusions, stress levels were low and uniform. In the analytical model, peak stresses were elevated at the edges of a rigid inclusion. In the finite element model, peak stresses were elevated at the edges of both inclusions, with minimal sensitivity to the wall distensibility and the size and shape of the inclusion. Presence of both a rigid and a soft inclusion enlarged the region of increased wall stress compared with either alone. In some configurations, the rigid inclusion reduced peak stress at the edge of the soft inclusion but simultaneously increased peak stress at the edge of the rigid inclusion and increased the size of the region affected. These findings suggest that the presence of a calcium deposit creates local increases in failure stress, and, depending on relative position to any neighboring lipid pools, it may increase peak stress and the plaque area at risk of mechanical failure.