Sympathomimetic toxicity, due, for example, to co- caine intoxication, not only increases myocardial oxygen demand but also induces coronary vasospasm and can cause infarction in young patients. Long-term cocaine use can cause premature development of IHD.68,69 Severe uncontrolled hypertension increases LV wall tension, leading to increased myocardial oxygen demand and decreased subendocardial perfusion. Hypertrophic cardiomyopathy and aortic stenosis can induce even more severe LV hypertrophy and resultant wall tension. Ventricular or supraventricular tachycardias are another cause of increased myocardial oxygen demand, but when paroxysmal these are difficult to diagnose. Anemia is the prototype for conditions that limit myocar- dial oxygen supply. Cardiac output rises when the hemoglo- bin drops to ,9 g/dL, and ST-T-wave changes (depression or inversion) can occur at levels ,7 g/dL. Hypoxemia resulting from pulmonary disease (eg, pneu- monia, asthma, chronic obstructive pulmonary disease, pul- monary hypertension, interstitial fibrosis, or obstructive sleep apnea) can also precipitate angina. Polycythemia, leukemia, thrombocytosis, and hypergammaglobulinemia are associated with increased blood viscosity that can decrease coronary artery blood flow and precipitate angina, even in patients without significant coronary stenoses. 2.1.6. Developing the Probability Estimate When the clinical evaluation is complete, the practitioner must determine whether the probability of IHD is sufficient to recommend further testing, which is often a standard exercise test. When the probability of disease is ,5%, further testing is usually not warranted because the likelihood of a false- positive test (ie, positive test in the absence of obstructive CAD) is actually higher than that of a true positive. On the other hand, when the exercise test is negative in a patient who has a very high likelihood of IHD on the basis of the history, there is a substantial chance that in reality the result is falsely negative. 