The index of microvascular resistance identifies patients with periprocedural myocardial infarction in elective percutaneous coronary intervention.

BACKGROUND: This study was designed to assess whether measurement of the index of microvascular resistance (IMR) could help prospectively identify patients who develop periprocedural myocardial infarction (PPMI). METHODS AND RESULTS: IMR was measured in 54 patients before and following percutaneous coronary intervention (PCI) in a culprit vessel with a PressureWire using the equation IMR = Pa(Hyp) × Tmn(Hyp) (Pd(Hyp)-Pw/Pa(Hyp)-Pw). IMR was also measured in an angiographically normal reference vessel. The relative pre-IMR ratio (rPIMR) defined as IMR Culprit divided by IMR Non-Culprit was also calculated. Troponin was sequentially sampled up to 24 h following PCI. Mean troponin post-PCI was 0.37±0.8 ng/ml. 33 (61%) patients fulfilled the criteria for PPMI. IMR pre-PCI was the most significant correlate of post-PCI troponin (r=0.43 p=0.001), however, the number of balloon inflations (r=0.3, p=0.02) and rPIMR (r=0.33 p=0.017) were also correlated. IMR pre-PCI was higher in patients with periprocedural myocardial infarction compared with patients without PPMI (IMR pre-PCI 21.2±2.1 PPMI vs 15.6±1.8 No PPMI, p=0.02). The strongest predictor of troponin post-PCI was IMR pre-PCI (ß 0.7, p=0.02). Both IMR pre- and rPIMR were predictive of PPMI (OR 11 (1.3 to 90.5) p=0.026, OR 1.09 (1 to 1.19) p=0.03, respectively). CONCLUSION: Microvascular function prior to PCI is an important determinant of PPMI. Measuring IMR pre-PCI and rPIMR may allow prospective identification of patients at risk of periprocedural myocardial infarction. Future studies in a larger cohort are required to establish the predictive ability of IMR in PPMI.

Percutaneous management of aortic stenosis in high-risk patients.

As the population ages, the prevalence of aortic stenosis is increasing. There is an unmet clinical need for the treatment of aortic stenosis in high-risk patients, who are often older, frail and have multiple comorbidities. Percutaneous aortic valve replacement (PAVR) is a new and innovative technique for the management of high-risk patients with aortic stenosis. There are currently two devices under evaluation in clinical trials in Australia: the CoreValve ReValving System and the Edwards SAPIEN valve. These devices are generally deployed retrogradely, mainly transfemorally or via the subclavian artery or, less commonly, transapically. Initial experience has been encouraging, with good short-term outcomes. However, there is a lack of long-term data. PAVR is presently only advocated for high-risk older patients with symptomatic aortic stenosis. Where PAVR lies in the treatment algorithm for aortic stenosis will be determined by randomised controlled trials, but for now it offers a genuine treatment alternative for high-risk patients.

Clozapine-induced cardiotoxicity: a clinical update.

Clozapine is a valuable drug for patients with treatment-resistant schizophrenia. Myocarditis is the most publicised cardiac complication of clozapine treatment, but cardiomyopathy and pericarditis have also been reported. Myocarditis has heterogeneous and non-specific presenting features, making it difficult to identify patients with clozapine-related myocarditis clinically. A high index of suspicion is required. The gold standard for diagnosis of myocarditis is an endomyocardial biopsy, but this is not a practical initial approach. Transthoracic echocardiography is a valuable, reproducible and widely available tool to assist in diagnosis of clozapine-induced cardiotoxicity. The level of B-type natriuretic peptide, a hormone secreted in response to ventricular wall stress, may be useful for evaluating patients with clozapine-induced cardiac dysfunction and may in the future be useful for screening asymptomatic patients. The mainstay of treatment of clozapine-induced cardiotoxicity is cessation of clozapine and provision of supportive care.