Cardiac stress test

Another main use is the radioisotope TlCl-201, with the relatively short half-life of about 73 hours, in cardiac stress tests to identify potential heart abnormalities. TlCl-201 has an ability to bind with the heart muscle, but only if the heart is receiving an adequate supply of... 

Answer The symptoms resemble those you remember from medical school for beriberi, but you fail to see the coimection. Then a light clicks on. If the patient were consuming most of his calories as alcohol, he may have a nutritional deficiency, a beriberi-Uke syndrome, as a result of insufficient intake of thiamine. You prescribe a daily vitamin tablet and admonish the patient to cut back on alcohol intake. At the next appointment, the edema is much better and the cardiac stress tests results are normal. He has joined Alcohohcs Anonymous and indicates that he is doing better. 

In another study, 63 of 122 patients had breathlessness during cardiac stress testing with adenosine but none had associated bronchospasm (34). Pre-test lung function did not predict the risk of breathlessness and neither chronic obstructive airways disease nor smoking increased the risk. The authors concluded that breathlessness during adenosine stress testing is not due to bronchospasm. 

Balan KK, Critchley M. Is the dyspnea during adenosine cardiac stress test caused by bronchospasm Am Heart J 2001 142(l) 142-5. 

The SPECT technique is primarily used for cardiovascular and brain imaging. Cardiac stress tests, using 201 1+ qj Tc labelled radiopharmaceuticals, amount in the U.S. to about 2 million a year. Brain tumors can be located by SPECT after intravenous injection of Na "Tc04, as brain tumors have a very high affinity for and slow release of Tc. In comparison, the uptake of Tc in brain infarcts is low and the release fast, and from healthy parts of the brain even faster thus various constrictions to the cerebral blood flow are easily located. A head scan can be made in 10 minutes and virtually instantaneously produces an image of the brain. 

The safety of G-CSF stimulation in patients with CAD has been questioned in two recent studies. Hill et al. [138] report the results of administration of 10 mcg/kg/day of G-CSF for 5 days in patients with chronic CAD n = 16). There was no clinical benefit as assessed by exercise stress testing and dobuta-mine cardiac MRI. Additionally two patients in the G-CSF group developed serious adverse events related to the therapy (one non-ST elevation MI one MI causing death). Zbinden et al. [139] also tested the efficacy of the same G-CSF dose in patients with chronic CAD ( = 7). The invasive endpoint collateral flow index was significantly better in the G-CSF treated patients when compared to the placebo group. However, two patients in the G-CSF treated group developed acute coronary syndrome during treatment. 

The effects of coenzyme Q10 on coronary artery disease and chronic stable angina are modest but appear promising. A theoretical basis for such benefit could be metabolic protection of the ischemic myocardium. Double-blind, placebo-controlled trials have demonstrated that coenzyme Q10 supplementation improved a number of clinical measures in patients with a history of acute myocardial infarction (AMI). Improvements have been observed in lipoprotein a, high-density lipoprotein cholesterol, exercise tolerance, and time to development of ischemic changes on the electrocardiogram during stress tests. In addition, very small reductions in cardiac deaths and rate of reinfarction in patients with previous AMI have been reported (absolute risk reduction 1.5%). 

The patient, a 63-year-old Caucasian female, was hospitalized on 4 April 2002 though 10 April 2002 for a non-ST segment elevation myocardial infarction (non-Q-wave MI per chart documentation). She had a negative adenosine stress test after the initial event. Her serum cardiac-specific troponin I (cTnl) concentration 24 hours after her onset of chest pain was 1.4 pg/L (upper limit of normal is 0.3 ng/mL), and her creatine kinase (CK) MB level was 12.5 pg/L (upper limit of normal 6.0 ng/mL). Three days post-event her cTnl level was 0.5 pg/L and her CK-MB level was 4.5 pg/L (Fig. 5-1). MB refers to one of the isoenzyme forms of CK found in serum. The form of the enzyme that occurs in brain (BB) does not usually get past the blood-brain barrier and therefore is not normally present in the serum. The MM and MB forms account for almost all of the CK in serum. Skeletal muscle contains mainly MM, with less than 2% of its CK in the MB form. MM is also the predominant myocardial creatine kinase and MB accounts for 10%-20% of creatine kinase in heart muscle. 

In 47 consecutive patients (mean age 64 years, 46 men) with three or more cardiovascular risk factors, intravenous dobutamine was given at a rate of 40micro-grams/kg/minute until the target heart rate was achieved, which took a mean of 11.6 minutes (4). Subjective sensations occurred in 49% of the patients (palpitation 21%, chest pain 6%, nausea 6%, headache 6%, dizziness 13%), while half the patients had abnormal cardiac rhythms (ventricular extra beats 38%, supraventricular tachycardia 10%, and non-sustained ventricular tachycardia 2%). The authors concluded that the safety and tolerability of this procedure is comparable to that of standard dobutamine stress testing, although its specificity and selectivity are still uncertain. 

The presence of an SAH associated with an ACS was considered to not have many clinical implications. However, the development of an SAH in the course of an inferior infarction (RCA or LCX) represents the involvement of at least two vessels, since LAD perfuses the superoanterior division. Recently, Biagini et al. (2005) reported that the presence of previous SAH implies worst prognosis. Patients with suspected IHD and LAH referred for stress test presented an increased risk for cardiac death. This risk is persistent after adjustment for major clinical data and abnormalities... 

In a broader unselected population referred for nuclear stress testing, Sharir et al. (6) found that the extent of reversible perfusion defect (as expressed by the summed difference score) was the best predictor of subsequent nonfatal myocardial infarction, and was best fit by an exponential curve. Among these patients, 26% had a history of myocardial infarction, and patients with nonischemic cardiomyopathies, valvular disease, or who underwent revascularization within 60 days were excluded. Importantly, even though ejection fraction most powerfully stratified the risk of cardiac death, in patients with an ejection fraction >30% the amount of perfusion defect provided incremental prognostic information. In patients with an ejection fraction of <30%, the rates of cardiac death were high (>4% per year) regardless of the amount of ischemia. 

For the growing number of patients with combined pulmonary hypertension and abnormal left ventricular hemodynamics, a careful hemodynamic study can help to delineate the subtleties of both diseases and response to therapies. Exercise catheterization is recommended in those patients with normal hemodynamics at rest, but with a pretest likelihood of PAH and/or other data suggesting exercise-induced symptoms, for instance, exercise echo or cardiopulmonary stress test. Unfortunately, to date there is no consensus as to the best exercise protocols for an appropriate hemodynamic assessment. Among those used include upright bicycle with neck pulmonary arterial (PA) lines at 75% predicted maximum exercise, supine bicycle, supine arm exercise, and supine volume loading. In all cases, it is essential to carefully measure PCWP, cardiac outputs, and PA pressures at consistent parts of the respiratory cycle, and not merely PA pressures. 

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