Clinical cardiology
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Clinical cardiology · Feb 1997
ReviewThe vital role of papillary muscles in mitral and ventricular function: echocardiographic insights.
The two left ventricular (LV) papillary muscles are small structures but are vital to mitral valve competence. Partial or complete rupture, complicating acute myocardial infarction, causes severe or even catastrophic mitral regurgitation, potentially correctable by surgery. Papillary muscle dysfunction is a controversial topic in that the role of the papillary muscle itself, in causing mitral regurgitation post infarction, has been seriously questioned; it is less confusing if this syndrome is attributed not only to papillary muscle but also to adjacent LV wall ischemia or infarction. ⋯ Papillary muscle hypertrophy accompanies LV hypertrophy of varied etiology and may have a significant role in producing dynamic late-systolic intra-LV obstruction in hypertrophic cardiomyopathy and other hyperdynamic hypertrophied LV chambers. All the above abnormalities can be adequately assessed by 2-D echocardiography and the Doppler modalities. In selected cases, transesophageal echocardiography can provide additional valuable data by improving visualization of papillary muscles and mitral apparatus.
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Clinical cardiology · Jul 1996
ReviewAngina pectoris refractory for conventional therapy--is neurostimulation a possible alternative treatment?
The treatment of angina pectoris as a symptom of coronary artery disease usually is focused on restoring the balance between oxygen demand and supply of the myocardium by administration of drugs interfering in heart rate, cardiac pre- and afterload, and coronary vascular tone. For nonresponders to drug therapy or for those with jeopardized myocardium, revascularization procedures such as coronary bypass surgery and percutaneous transluminal coronary angioplasty are at hand. However, the atherosclerotic process is not stopped by these therapies and, at longer terms, angina may recur. ⋯ For these patients, neurostimulation has been described repeatedly as an effective and safe therapy. The mechanism of action of neurostimulation is not completely known, but recent studies suggest an anti-ischemic effect, exerted through changes in myocardial blood flow. As soon as its safety is sufficiently established, it may become a useful alternative in the treatment of refractory angina pectoris.
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Clinical cardiology · Sep 1995
ReviewAdvanced cardiac life support: update on recent guidelines and a look at the future.
The objectives of this article are to provide an update of the American Heart Association (AHA) 1992 National Conference guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiac care and to review the investigation and development of new methods of CPR which may be considered in future recommendations. Despite an organized approach to sudden cardiac arrest, survival in patients receiving CPR is in the range of 5-15%. The new AHA guidelines recommend standard manual CPR performed at a rate of 80-100 compressions/min and organized algorithms of advanced cardiac life support. ⋯ Each of these techniques offers unique advantages when compared with standard manual cardiopulmonary resuscitation. The 1992 National Conference recommendations provide a rational framework for the resuscitation of cardiac arrest victims. New methods of cardiopulmonary resuscitation are now available and investigation into these methods continues.(ABSTRACT TRUNCATED AT 250 WORDS)
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Clinical cardiology · Aug 1995
ReviewPreoperative strategies to assess cardiac risk before noncardiac surgery.
The strategies recommended in the preoperative cardiac risk assessment prior to major vascular and nonvascular surgery are reviewed. The role of clinical evaluation, noninvasive stress testing (exercise test, stress myocardial perfusion imaging, stress echocardiography), and Holter monitoring during the preoperative evaluation are outlined and the value of intervention based on the use of each test is discussed. Recommended strategies to evaluate patients based on their clinical risk markers in addition to the results of the noninvasive risk assessment are presented.
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Clinical cardiology · May 1995
Review Case ReportsTorsade de pointes caused by high-dose intravenous haloperidol in cardiac patients.
Intravenous haloperidol is the agent of choice for controlling severe agitated delirium in seriously ill cardiac patients in many institutions. Prior reports have proposed that high-dose intravenous haloperidol may be without untoward effects in these patients. Recently, however, a few reports of significant QTc prolongation and torsade de pointes as complications of high-dose intravenous haloperidol therapy have appeared. ⋯ Neither electrolyte imbalance, therapy with other cardiac drugs, bradycardia, ischemia, left ventricular dysfunction, nor other known cause of torsade was present in these patients. It is hypothesized that QTc prolongation and torsade likely are idiosyncratic, unpredictable reactions to high-dose haloperidol in select patients. Careful serial electrocardiographic monitoring and prompt discontinuation of the drug should suffice to prevent this relatively uncommon, life-threatening complication of high-dose intravenous haloperidol.