The use of iodinated contrast agents for angiography dates back to the 1920s. With over 75 million contrast-requiring procedures performed annually worldwide, it is important to understand the risk factors, pathogenesis, diagnosis, prevention, and treatment of adverse reactions caused by iodinated contrast media (ICM). As contrast media have evolved from ionic, high-osmolality to nonionic, low-osmolality formulations the risk of reactions has decreased over time; however, no pretreatment protocol has been shown to eliminate all repeat reactions. Clinical alertness and early recognition of adverse reactions is of paramount importance and key for appropriate management of these patients. In this article, we review the most recent literature regarding adverse reactions to ICM and provide an insight into the pathogenesis, clinical presentation, pretreatment, and management of contrast-related reactions.

OBJECTIVES This study postulated that antihypertensive therapy with renin-angiotensin-aldosterone system (RAAS) inhibition may mitigate vascular endothelial growth factor inhibitor (VEGFi)–mediated increases in blood pressure more effectively than other antihypertensive medications in patients receiving VEGFi therapy. BACKGROUND VEGFi therapy is commonly used in the treatment of cancer. One common side effect of VEGFi therapy is elevated blood pressure. Evidence suggests that the RAAS may be involved in VEGFi-mediated increases in blood pressure. METHODS This retrospective cohort analysis was performed using a de-identified version of the electronic health record at Vanderbilt University Medical Center in Nashville, Tennessee. Subjects with cancer who were exposed to VEGFi therapy were identified, and blood pressure and medication data were extracted. Changes in mean systolic and diastolic blood pressure in response to VEGFi therapy in patients receiving RAAS inhibitor (RAASi) therapy before VEGFi initiation were compared with changes in mean systolic and diastolic blood pressure in patients not receiving RAASi therapy before VEGFi initiation. RESULTS Mean systolic and diastolic blood pressure rose in both groups after VEGFi use; however, patients who had RAASi therapy before VEGFi initiation had a significantly lower increase in systolic blood pressure as compared with patients with no RAASi therapy (2.46 mm Hg [95% confidence interval: 0.7 to 4.2] compared with 4.56 mm Hg [95% confidence interval: 3.5 to 5.6], respectively; p = 0.034). CONCLUSIONS In a real-world clinical population, RAASi therapy before VEGFi initiation may ameliorate VEGFi-mediated increases in blood pressure. Randomized clinical trials are needed to further our understanding of the role of RAASi therapy in VEGFi-mediated increases in blood pressure. (J Am Coll Cardiol CardioOnc 2019;1:14–23)

W hen massive pulmonary embolism (PE) results in hemodynamic compromise, the mortality rate is 50% to 100%.1,2 In these emergent cases, the current practice guidelines include immediate thrombolysis, in the absence of contraindications such as hemorrhagic stroke.3,4 However, there are no clear therapeutic guidelines for treating high-risk PE when thrombolytic therapy is said to be contraindicated. In such cases, investigators have proposed that the contraindications be viewed as relative rather than absolute.2,4 We discuss our therapeutic decisions, and their results, in the case of a patient who had massive PE and a recent history of hemorrhagic stroke. Case ReportIn February 2012, a 60-year-old woman who had sustained a hemorrhagic cerebrovascular accident (CVA) 8 weeks earlier presented with acute lethargy, blurred vision, hypotension, and bradycardia. An electrocardiogram revealed a junctional rhythm. A bedside echocardiogram revealed right ventricular (RV) dilation and dysfunction, and pulmonary hypertension. Further evaluation yielded deep vein thrombosis in the right lower extremity, and results of a ventilation/perfusion scan suggested an intermediate probability of PE. Anticoagulation with heparin was initiated for PE with hemodynamic compromise, and dobutamine was started for RV failure. The placement of an inferior vena cava filter was planned.On the 3rd day of hospitalization, the patient had 2 episodes of cardiac arrest with pulseless electrical activity. After the first resuscitation, an electrocardiogram showed atrial tachycardia, right bundle branch block, a large Q wave in lead III, and mild STsegment elevation. A chest radiograph revealed left-lower-lobe atelectasis that obscured the left border of the heart, and an area of aerated but hypovolemic lung that was consistent with a Westermark sign. A bedside echocardiogram showed worsening RV dilation and systolic dysfunction, pulmonary hypertension, and a severely under-filled left ventricle (Fig. 1).

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