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Introduction For patients with esophageal cancer undergoing neoadjuvant chemoradiation (CRT) followed by surgical resection, complete histopathologic response (pCR) is associated with favorable overall survival (OS). The aim of this study was to evaluate the correlation between 18 F-fluorodeoxyglucose positron emission tomography (FDG PET) response to neoadjuvant CRT and pCR. Methods Maximum standardized uptake values and standardized uptake ratios (SURs) were measured before and after CRT. SUR was normalized to liver uptake and mediastinal blood pool uptake. FDG PET complete response was defined as metabolic activity normalization to hepatic and blood pool activity. The correlation between FDG PET parameters and pCR was examined through logistic regression analyses. Results In total, 193 patients were monitored for a median of 3.6 years after initiation of CRT. Most tumors were adenocarcinoma (85%) and stage T3 (75%). Complete FDG PET response and pCR occurred in 27% and 34% of patients, respectively. Histologic findings, chemotherapy type, tumor stage, and radiation dose were not significantly associated with complete radiographic response. The rates of pCR in patients with and without radiographic complete response were 42% and 31% ( p = 0.17), respectively. No predictive correlation was found between pCR and change in maximum standardized uptake value ( p = 0.25), in SUR normalized to blood pool uptake ( p = 0.20), or in SUR normalized to liver uptake ( p = 0.15). The 5-year OS rate was 46% for patients with a complete FDG PET response versus 44% without a complete response ( p = 0.78). The 5-year OS rate of patients who achieved pCR was 49% versus 43% for patients with residual tumor ( p = 0.04). Conclusion For patients with esophageal cancer who received neoadjuvant chemoradiation, pretreatment and posttreatment FDG PET parameters did not correlate with pCR or OS.

Measurement of cardiac output, arteriovenous oxygen difference, and oxygen uptake in patients with heart failure may be subject to technical and biologic inaccuracies. We measured these 3 variables in 16 patients with chronic heart failure at rest and during exercise. When cardiac output was measured by thermodilution and compared with values calculated by the Fick principle, there was a significant correlation at rest (r = 0.91, p less than 0.001) and at exercise (r = 0.93, p less than 0.001). When the arteriovenous oxygen difference was measured by spectrophotometry of arterial and mixed venous samples and compared with values calculated by the Fick principle, there was a significant correlation at rest (r = 0.80, p less than 0.01) and at exercise (r = 0.76, p less than 0.01). When oxygen uptake was measured from expired gas analysis and compared with values calculated by the Fick principle, there was a significant correlation at rest (r = 0.84, p less than 0.01) and at exercise (r = 0.94, p less than 0.001). In addition, 10 patients received vasodilator treatment which increased cardiac output and decreased the arteriovenous oxygen difference at rest and exercise. There was no significant difference between measured and calculated values for the 3 variables under those additional conditions. It is concluded that despite technical and biologic difficulties, cardiac output, arteriovenous oxygen difference, and oxygen uptake, when calculated from Fick's principle, yield results equivalent to direct measurement.

Intermittent vasospasm and/or platelet aggregation may play an important role in producing transient coronary artery obstruction leading to an unstable ischemic syndrome. To determine whether intravenous infusion of prostaglandin E1 (PGE1) a known coronary vasodilator and inhibitor of platelet aggregation, produces salutary effects in unstable angina, we evaluated its effects in 19 patients with an unstable acute ischemic syndrome. PGE1 produced a significant decrease in the number of episodes of rest angina (p less than 0.001) and eliminated the need for intravenous nitroglycerin and morphine in 10 patients. These salutary clinical effects were associated with a significant (p less than 0.05) reduction in mean arterial pressure, mean pulmonary artery pressure, mean pulmonary capillary wedge pressure, and the double product, without a reduction in the endocardial perfusion gradient (aortic diastolic blood pressure--mean pulmonary capillary wedge pressure). Adverse effects were generally minor and easily controlled. Thus PGE1 infusion may be of value in the treatment of acute unstable ischemic syndromes.

The effects of acute and chronic oral administration of the vasodilator minoxidil on hemodynamics, oxygen consumption, exercise performance, and clinical status were investigated in 10 patients with severe, chronic heart failure refractory to digitalis and diuretic therapy. The cardiac index was 1.99 +/- 0.38 liters/min/m2 at rest and 2.88 +/- 0.79 at symptom-limited maximal exercise on conventional therapy, compared with 2.64 +/- 0.33 liters/min/m2 at rest and 3.55 +/- 0.84 at maximal exercise after short-term minoxidil administration (p less than 0.02, control versus minoxidil at both rest and exercise). Stroke volume was increased after minoxidil treatment, without significant effect on heart rate. Systemic vascular resistance was decreased by minoxidil from 2,050 +/- 722 to 1,325 +/- 374 dynes . s/cm-5 at rest and from 1,500 +/- 830 to 1,206 +/- 589 dynes . s/cm-5 at maximal exercise (p = 0.01, control versus minoxidil). No significant effect was observed on left ventricular filling, right atrial, or mean pulmonary arterial pressure, but pulmonary vascular resistance decreased both at rest and on exercise (p less than 0.05). Maximal exercise oxygen consumption increased from 8.9 +/- 3.2 ml/kg/min on conventional therapy to 10.5 +/- 2.4 on minoxidil therapy (p less than 0.03), median maximal exercise work load increased from 25 to 50 W and medium exercise duration increased from 6.0 to 9.0 minutes. On chronic minoxidil administration all 5 patients who completed a scheduled 6 week follow-up showed symptomatic improvement. However, worsening edema developed in all patients, requiring increased diuretic dosage and close supervision. Symptoms of ischemic heart disease worsened in 2 of 10 patients. We tentatively conclude that minoxidil may be a useful vasoactive agent in the pharmacologic therapy of severe chronic heart failure.