Publications

Successful reperfusion of an infarct-related coronary artery by primary percutaneous intervention or fibrinolysis during acute ST-elevation myocardial infarction (STEMI) does not always restore myocardial tissue perfusion, a phenomenon termed "no-reflow." Herein we discuss the pathophysiology of this highly prevalent phenomenon and highlight the most salient aspects of its clinical diagnosis and management as well as the limitations of presently used methods. There is a great need for understanding the dynamic nature of no-reflow, as its occurrence is associated with poor cardiovascular outcomes. The no-reflow phenomenon may lend an explanation to the lack of further improvements in in-hospital mortality in STEMI patients despite decreases in door-to-balloon time. Hence, no-reflow potentially presents an important target for investigators interested in improving outcomes in STEMI.

More than four decades ago, the United States Surgeon General issued a warning regarding the medical problems of marijuana smoking, including cardiac toxicity. Since then, many reports have described atrial fibrillation, ventricular tachycardia, acute coronary syndromes, and cardiac arrest temporally related to marijuana use. The subjects were quite young, with no significant cardiovascular risk factors, with the only obvious trigger being marijuana use. Despite these strong signals, the drug is now legalized for recreational use in many states. We believe the time has come to conduct definitive studies about the safety of marijuana before this trend moves to the rest of the nation.

INTRODUCTION: Hyperkalemia (potassium >5.0 mEq/L) affects heart failure patients with renal disease regardless of the use of renin-angiotensin-aldosterone system inhibitors (RAASi). The open-label TOURMALINE study showed that patiromer, a sodium-free, nonabsorbed potassium binder, lowers serum potassium of hyperkalemic patients similarly when given with or without food; unlike prior studies, patients were not required to be taking RAASi. We conducted post hoc analyses to provide the first report of patiromer in patients not taking RAASi.

METHODS: Hyperkalemic patients received patiromer, 8.4 g/d to start, adjusted to achieve and maintain serum potassium of 3.8 to 5.0 mEq/L. If taking RAASi, stable doses were required. The primary end point was the proportion of patients with serum potassium 3.8 to 5.0 mEq/L at week 3 or 4. This analysis presents data by patients taking or not taking RAASi.

RESULTS: Demographics and baseline characteristics were similar in patients taking (n = 67) and not taking RAASi (n = 45). Baseline mean (SD) serum potassium was 5.37 (0.37) mEq/L and 5.42 (0.43) mEq/L in patients taking and not taking RAASi, respectively. Mean (SD) daily patiromer doses were similar (10.7 [3.2] and 11.5 [4.0] g, respectively). The primary end point was achieved in 85% (95% confidence interval [CI]: 74-93) of patients taking RAASi and in 84% (95% CI: 71-94) of patients not taking RAASi. From baseline to week 4, the mean (SE) change in serum potassium was -0.67 (0.08) mEq/L in patients taking RAASi and -0.56 (0.10) mEq/L in patients not taking RAASi (both P < .0001 vs baseline, P = nonsignificant between groups). Adverse events were reported in 26 (39%) patients taking RAASi and 25 (54%) not taking RAASi; the most common adverse event was diarrhea (2% and 11%, respectively; no cases were severe). Five patients (2 taking RAASi) reported 6 serious adverse events; none considered related to patiromer.

CONCLUSIONS: Patiromer was effective and generally well-tolerated for hyperkalemia treatment, whether or not patients were taking RAAS inhibitors.

Inability to predict short-term cardiovascular (CV) events and take immediate preemptive actions has long been the Achilles heel of cardiology. However, certain triggers of these events have come to light. Although these triggers are nonspecific and are part of normal life, studying their temporal relationship with the onset of CV events provides an opportunity to alert high-risk atherosclerotic patients who may be most vulnerable to such triggers, the "vulnerable patient". Herein, we review the literature and shed light on the epidemiology and underlying pathophysiology of different triggers. We describe that certain adrenergic triggers can precipitate a CV event within minutes or hours; whereas triggers that elicit an immune or inflammatory response such as infections may tip an asymptomatic "vulnerable patient" to become symptomatic days and weeks later. In conclusion, healthcare providers should counsel high-risk CV patients (e.g., in secondary prevention clinics or those with coronary artery Calcium >75th percentile) on the topic, advise them to avoid such triggers, take protective measures once exposed, and seek emergency care immediately after becoming symptomatic after such triggers. Furthermore, clinical trials targeting triggers (prevention or intervention) are needed.