Chiefs’ Inquiry Corner — 7/26/21

 Nonselective beta blockers (specifically propranolol) were first studied in the early 1980s as agents that may have a role in decreasing portal venous pressure with the downstream effect of reducing re-bleeding events in patients with cirrhosis presenting with gastrointestinal hemorrhage. Cardioselective beta-blockers have been shown to be less effective (in small studies) compared to nonselective agents; it is thought that the cardioselective agents have a greater effect on decreasing cardiac output with less effect directly on portal pressures. One study looking at a direct comparison between carvedilol and propranolol did show that carvedilol had a substantial effect on lowering the hepatic venous pressure gradient; however, these effects (though potentially greater than effects of propranolol) were offset by the subsequent decrease in mean arterial pressure and subsequent systemic hypotension.

References: 1. Propranolol for Prevention of Recurrent Gastrointestinal Bleeding in Patients with Cirrhosis: A Controlled Study 2. Randomized comparison of long-term carvedilol and propranolol administration in the treatment of portal hypertension in cirrhosis

 Tachycardia-induced cardiomyopathy is thought to be a rate-dependent cardiomyopathy. Though it may take months to years to see the effects of underlying arrhythmia (most commonly supraventricular tachycardias rather than ventricular), patients with higher rates likely develop the cardiomyopathy earlier. Some evidence suggests that it typically manifests in patients with chronic tachycardia occurring at least 10-15% of the day. The specific heart rate threshold itself has not been consistently demonstrated, but generally a rate >100 seems to place patients at risk. In addition to the heart rate itself, the contribution of asynchronous myocardial contraction has been suggested. The greatest left ventricular ejection fraction recovery usually occurs at least 1 month after achieving control of the arrhythmia, with the majority achieving near-normalization at 3 month follow-up. A minority of patients may see recovery continue up to 1 year.

References: 1. Tachycardia-induced cardiomyopathy 2. Pathophysiology, diagnosis and treatment of tachycardiomyopathy

 In previous studies, high sensitivity troponin (ie troponin-HS) assays have been shown to improve the diagnosis of myocardial infarction in patients without kidney impairment. However, elevations in troponin levels are common in patients with kidney impairment and interpretation of troponin-HS in this group is uncertain. A recent stepped-wedge cluster-randomized clinical trial (High-STEACS) evaluated the use of troponin-HS assays in patients with kidney impairments and suspected acute coronary syndrome. They examined a primary outcome of subsequent type 1 vs type 4b myocardial infarction or cardiovascular death within 1 year after an index presentation . The outcome was compared between using the classic TnI versus utilization of troponin-HS. The trial found a 6 fold increase of troponin-HS as kidney function declined from an eGFR of 90 to less than 30 mL/min/1.73m2. However, the proportion attributable to a type 1 myocardial infarction halved. The study found that while troponin-HS is effective at ruling out early MI in patients with kidney impairment, its use did not improve outcomes in patients with elevated levels. Further research is needed to evaluate the utility of troponin-HS for this heterogeneous group.

References: Use of High-Sensitivity Cardiac Troponin in Patients With Kidney Impairment