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An estimated 16 million people in the United States have coronary artery disease (CAD), and approximately 325,000 people die annually from cardiac arrest. About two-thirds of unexpected cardiac deaths occur without prior recognition of cardiac disease. A vast majority of these deaths are attributable to the rupture of 'vulnerable atherosclerotic plaques'. Clinically, plaque vulnerability is typically assessed through imaging techniques, and ruptured plaques leading to acute myocardial infarction are treated through angioplasty or stenting. Despite significant advances, it is clear that current imaging methods are insufficiently capable for elucidating plaque composition--which is a key determinant of vulnerability. Further, the exciting improvement in the treatment of CAD afforded by stenting procedures has been buffered by significant undesirable host-implant effects, including restenosis and late thrombosis. Nanotechnology has led to some potential solutions to these problems by yielding constructs that interface with plaque cellular components at an unprecedented size scale. By leveraging the innate ability of macrophages to phagocytose nanoparticles, contrast agents can now be targeted to plaque inflammatory activity. Improvements in nano-patterning procedures have now led to increased ability to regenerate tissue isotropy directly on stents, enabling gradual regeneration of normal, physiologic vascular structures. Advancements in immunoassay technologies promise lower costs for biomarker measurements, and in the near future, may enable the addition of routine blood testing to the clinician's toolbox--decreasing the costs of atherosclerosis-related medical care. These are merely three examples among many stories of how nanotechnology continues to promise advances in the diagnosis and treatment of vulnerable atherosclerotic plaques.

Respiratory and pharmacologic interventions are used during auscultation of heart sounds. These same principles may be utilized in the echocardiography laboratory to aid diagnosis. Four physical maneuvers and one pharmacologic intervention performed in the echocardiography laboratory are described. A brief discussion of applications in specific clinical situations is then presented. The Valsalva maneuver involves having the patient inspire deeply followed by a forceful exhalation against a closed glottis for approximately 10 seconds. Placing the hand on the patient’s abdomen by the examiner provides a force for the patient to strain against and ensures that the abdominal muscles are tightening.1 Some patients who have difficulty with this may find it best to insert their index finger in the mouth and attempt to blow out with lips sealed. Alternatively, the patient may blow into a manometer to maintain 40 mmHg or more.2 The Valsalva maneuver involves the following four phases

Patient-prosthetic aortic valve mismatch (PPM) is a clinical diagnosis in which an aortic prosthetic valve is normal structurally, but hemodynamically functions as aortic stenosis, with higher prosthetic valve gradients than would be expected for that particular valve.1,2 The prosthetic valve functions as designed but hemodynamics are less than ideal compared with a native valve. The predominant hemodynamic consequence of PPM is generation of an abnormally high mean pressure gradient (MPG), which may become evident only during or after exercise. The MPG is related to flow (Q) and prosthetic effective orifice area (EOA) by the following relationship