Clinical Characteristics and Outcomes Among People Living With HIV Undergoing Percutaneous Coronary Intervention: Insights From the Veterans Affairs Clinical Assessment, Reporting, and Tracking Program.

Background Clinical characteristics and outcomes in people living with HIV (PLWH) undergoing percutaneous coronary intervention (PCI) remain poorly described. We sought to compare real-world treatment of coronary artery disease, as well as patient and procedural factors and outcomes after PCI between PLWH and uninfected controls. Methods and Results We utilized procedural registry data from the Veterans Affairs Clinical Assessment, Reporting, and Tracking Program between January 1, 2009 and December 31, 2019 to analyze patients with obstructive coronary artery disease on angiography. In the PCI subgroup, we used inverse probability of treatment weighting and applied Cox proportional hazards to evaluate the association of HIV serostatus with outcomes, including all-cause mortality at 5 years. Among 184 310 patients with obstructive coronary artery disease, treatment strategy was similar between PLWH and controls-35.7% versus 34.2% PCI, 13.6% versus 15% coronary artery bypass grafting, and 50.7% versus 50.8% medical therapy. The PCI cohort consisted of 546 (0.9%) PLWH and 56 811 (99.1%) controls. PLWH undergoing PCI had well-controlled HIV disease, and compared with controls, were younger, more likely to be Black, had fewer traditional risk factors, more acute coronary syndrome, less extensive coronary artery disease, and similar types of stents and P2Y12 therapy. However, PLWH experienced worse survival as early as 6 months post-PCI, which persisted over time and amounted to a 21% increased mortality risk by 5 years (hazard ratio, 1.21 [95% CI, 1.03-1.42; P=0.02]). Conclusions Despite well-controlled HIV disease, a more favorable overall cardiovascular risk profile, and similar PCI procedural metrics, PLWH still have significantly worse long-term survival following PCI than controls.

Fractional Flow Reserve in End-Stage Liver Disease.

Fractional flow reserve (FFR) determines the functional significance of epicardial stenoses assuming negligible venous pressure (Pv) and microvascular resistance. However, these assumptions may be invalid in end-stage liver disease (ESLD) because of fluctuating Pv and vasodilation. Accordingly, all patients with ESLD who underwent right-sided cardiac catheterization and coronary angiography with FFR as part of their orthotopic liver transplantation evaluation between 2013 and 2018 were included in the present study. Resting mean distal coronary pressure (Pd)/mean aortic pressure (Pa), FFR, and Pv were measured. FFR accounting for Pv (FFR - Pv) was defined as (Pd - Pv)/(Pa - Pv). The hyperemic effect of adenosine was defined as resting Pd/Pa - FFR. The primary outcome was all-cause mortality at 1 year. In 42 patients with ESLD, 49 stenoses were interrogated by FFR (90% were <70% diameter stenosis). Overall, the median model for ESLD score was 16.5 (10.8 to 25.5), FFR was 0.87 (0.81 to 0.94), Pv was 8 mm Hg (4 to 14), FFR-Pv was 0.86 (0.80 to 0.94), and hyperemic effect of adenosine was 0.06 (0.02 to 0.08). FFR-Pv led to the reclassification of 1 stenosis as functionally significant. There was no significant correlation between the median model for ESLD score and the hyperemic effect of adenosine (R = 0.10). At 1 year, 13 patients had died (92% noncardiac in etiology), and patients with FFR ≤0.80 had significantly higher all-cause mortality (73% vs 17%, p = 0.001. In conclusion, in patients with ESLD who underwent orthotopic liver transplantation evaluation, Pv has minimal impact on FFR, and the hyperemic effect of adenosine is preserved. Furthermore, even in patients with the predominantly angiographically-intermediate disease, FFR ≤0.80 was an independent predictor of all-cause mortality.

Fatal Rhabdomyolysis in a COVID-19 Patient on Rosuvastatin.

It is well-established by now that COVID-19 can have a wide variety of neuromuscular manifestations, including rhabdomyolysis. Weakness and elevated creatinine kinase (CK) have been documented as the initial presentation of COVID-19. Myopathy from statin use has also been well-established since the introduction of this class of medication, and the common pathologic mechanism of both entities may have been mitochondrial dysfunction. We present here the case of a COVID-19 patient on rosuvastatin who developed rhabdomyolysis with CK above 1,000,000 units/L. The patient did not present with any respiratory difficulty and responded poorly to treatment, resulting in his untimely demise. COVID-19 may have accentuated an otherwise survivable condition by means of extra stress on mitochondrial homeostasis. Understanding the actual mechanism will be important in the development and utilization of medications in the fight against COVID-19.

Incidence, Predictors, and Outcomes of New-Onset Left Ventricular Systolic Dysfunction After Orthotopic Liver Transplantation.

BACKGROUND: Adverse cardiovascular events after liver transplantation (LT) are relatively common and are a significant source of early mortality. Although new-onset systolic dysfunction after LT is a reported phenomenon, there is little data regarding its incidence, risk factors, and outcomes. METHODS AND RESULTS: This single-center retrospective study included all adult patients from January 2002 to March 2015 with deceased-donor LT and available preoperative transthoracic echocardiograms (TTEs). In total, 1,760 patients were included in the study, 602 (34.2%) of whom had a postoperative TTE. The primary end point was development of new-onset cardiomyopathy, defined as a new left ventricular ejection fraction (LVEF) of <40% within 180days of transplant. Sixty-nine (11.4%) of the patients who received post-LT TTE had a reduction in LVEF to <40% within 6 months. Clinical parameters of donor and recipient did not show significant impact on development of post-LT LV systolic dysfunction (LVSD). Presence of wall motion abnormalities (P = .004) on preoperative TTE was predictive of development of post-LT LVSD. These patients did not have longer hospitalizations, but they had worse survival. CONCLUSIONS: Post-LT LV systolic dysfunction occurs at higher rates than previously suspected and may develop more frequently in patients with underlying cardiac structural abnormalities, which appear to adversely affect post-LT survival.

Orbital and rotational atherectomy during percutaneous coronary intervention for coronary artery calcification.

Severe coronary artery calcification (CAC) increases the complexity of percutaneous coronary intervention (PCI) by inhibiting optimal stent expansion, leading to an increased risk of death, myocardial infarction, repeat revascularization, and stent thrombosis. Coronary atherectomy modifies and debulks calcified plaque to facilitate PCI. Although there is no clear consensus, and further studies are needed, the decision to perform atherectomy should be based upon the presence of fluoroscopic CAC or with the use of intravascular imaging. The management of CAC in the modern era relies on rotational and orbital atherectomy to prepare the lesion to facilitate stent delivery and optimal expansion. While the two technologies differ in equipment, technique, and mechanism of action, the available literature suggests similar efficacy and safety of the two systems, although head-to-head comparisons are limited. While rotational and orbital atherectomy have been shown to have excellent procedural success in terms of facilitating stent delivery, no system has been shown to reduce long-term major adverse cardiovascular events, although the definitive trial for orbital atherectomy has not been completed. Additional trials are needed to find the population who would derive the most benefit of atherectomy and to compare the two systems in a prospective manner.

Changes in Cardiovascular Disease Risk Factors With Immediate Versus Deferred Antiretroviral Therapy Initiation Among HIV-Positive Participants in the START (Strategic Timing of Antiretroviral Treatment) Trial.

INTRODUCTION: HIV infection and certain antiretroviral therapy (ART) medications increase atherosclerotic cardiovascular disease risk, mediated, in part, through traditional cardiovascular disease risk factors. METHODS AND RESULTS: We studied cardiovascular disease risk factor changes in the START (Strategic Timing of Antiretroviral Treatment) trial, a randomized study of immediate versus deferred ART initiation among HIV-positive persons with CD4+ cell counts >500 cells/mm3. Mean change from baseline in risk factors and the incidence of comorbid conditions were compared between groups. The characteristics among 4685 HIV-positive START trial participants include a median age of 36 years, a CD4 cell count of 651 cells/mm3, an HIV viral load of 12 759 copies/mL, a current smoking status of 32%, a median systolic/diastolic blood pressure of 120/76 mm Hg, and median levels of total cholesterol of 168 mg/dL, low-density lipoprotein cholesterol of 102 mg/dL, and high-density lipoprotein cholesterol of 41 mg/dL. Mean follow-up was 3.0 years. The immediate and deferred ART groups spent 94% and 28% of follow-up time taking ART, respectively. Compared with patients in the deferral group, patients in the immediate ART group had increased total cholesterol and low-density lipoprotein cholesterol and higher use of lipid-lowering therapy (1.2%; 95% CI, 0.1-2.2). Concurrent increases in high-density lipoprotein cholesterol with immediate ART resulted in a 0.1 lower total cholesterol to high-density lipoprotein cholesterol ratio (95% CI, 0.1-0.2). Immediate ART resulted in 2.3% less BP-lowering therapy use (95% CI, 0.9-3.6), but there were no differences in new-onset hypertension or diabetes mellitus. CONCLUSIONS: Among HIV-positive persons with preserved immunity, immediate ART led to increases in total cholesterol and low-density lipoprotein cholesterol but also concurrent increases in high-density lipoprotein cholesterol and decreased use of blood pressure medications. These opposing effects suggest that, in the short term, the net effect of early ART on traditional cardiovascular disease risk factors may be clinically insignificant." CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT00867048.

New medications for heart failure.

Heart failure is common and results in substantial morbidity and mortality. Current guideline-based therapies for heart failure with reduced ejection fraction, including beta blockers, angiotensin converting enzyme (ACE) inhibitors, and aldosterone antagonists aim to interrupt deleterious neurohormonal pathways and have shown significant success in reducing morbidity and mortality associated with heart failure. Continued efforts to further improve outcomes in patients with heart failure with reduced ejection fraction have led to the first new-in-class medications approved for heart failure since 2005, ivabradine and sacubitril/valsartan. Ivabradine targets the If channels in the sinoatrial node of the heart, decreasing heart rate. Sacubitril/valsartan combines a neprilysin inhibitor that increases levels of beneficial vasodilatory peptides with an angiotensin receptor antagonist. On a background of previously approved, guideline-directed medical therapies for heart failure, these medications have shown improved clinical outcomes ranging from decreased hospitalizations in a select group of patients to a reduction in all-cause mortality across all pre-specified subgroups. In this review, we will discuss the previously established guideline-directed medical therapies for heart failure with reduced ejection fraction, the translational research that led to the development of these new therapies, and the results from the major clinical trials of ivabradine and sacubitril/valsartan.

Facilitated patent haemostasis after transradial catheterisation to reduce radial artery occlusion.

AIMS: This study sought to evaluate the feasibility of a rapid deflation technique (RDT) after transradial catheterisation to achieve patent haemostasis and to assess whether this could reduce radial artery occlusion (RAO). Ensuring patent haemostasis is the most important factor in reducing RAO. The use of larger sheath sizes and antiplatelet and antithrombotic agents limits achieving patent haemostasis immediately after transradial intervention. METHODS AND RESULTS: A feasibility assessment was first performed in 105 patients to assess whether RDT could be performed safely and consistently achieve patent haemostasis after transradial catheterisation. Prospective data were then collected on 201 patients who underwent either rapid or standard deflation technique and had RAO assessment at 24 hours. Acute coronary syndrome was the indication for transradial catheterisation in 62.7% of patients. Baseline patent haemostasis increased from 40% to 95% after RDT. RAO at 24 hours was seen in two (2.0%) patients in the RDT group and 15 (14.9%) in the standard deflation group (OR 0.117; 95% CI: 0.026 to 0.526, p=0.005). Other independent predictors of RAO included body surface area (OR 0.022; 95% CI: 0.002 to 0.273, p=0.003) and male sex (OR 0.298; 95% CI: 0.108 to 0.824, p=0.020). No significant difference was found in safety outcomes: need to re-inflate compression band (2% versus 1.8%) or haematoma (0% versus 0.9%). CONCLUSIONS: Rapid deflation of the compression band after transradial catheterisation is a safe and effective method of achieving patent haemostasis that reduces RAO.

Impact of peripheral vascular disease on short- and long-term outcomes in patients undergoing non-emergent percutaneous coronary intervention in the drug-eluting stent era.

OBJECTIVES: This study sought to compare short- and long-term (4-year) outcomes in patients with and without peripheral vascular disease (PVD) following non-emergent percutaneous coronary intervention (PCI) in current clinical practice. BACKGROUND: Patients with PVD undergoing coronary revascularization have high rates of adverse short-term outcomes. However, the long-term clinical outcomes of patients with PVD undergoing PCI in the contemporary drug-eluting stent (DES) era have not been well characterized. METHODS: The 2004/2005 Cornell Angioplasty Registry database was used to evaluate the in-hospital and long-term clinical outcomes in patients undergoing non-emergent (urgent or elective) PCI. A total of 2455 study patients were examined. We excluded patients presenting with an ST-elevation myocardial infarction (MI) ≤ 24 hours, hemodynamic instability/shock, thrombolytic therapy ≤ 7 days, or renal insufficiency (creatinine ≥ 4 mg/dL). Mean clinical follow-up was 4.4 ± 1.1 years. RESULTS: Of the 2455 patients, a total of 173 (7%) had PVD and 2282 (93%) had no reported history of PVD. DESs were used in 87% of the PCIs. The incidence of in-hospital death (1.8% vs 0.1%; P=.006) was greater in the PVD group, whereas postprocedural MI (6.4% vs 6.8%; P=.810) and major adverse cardiovascular event rates including death, stroke, emergent coronary artery bypass graft/PCI, and MI (8.7% vs 7.0%; P=.360) were similar in the PVD versus no PVD groups. Long-term Kaplan-Meier survival (89.2% vs 76.2%; P<.001) was significantly higher in patients without PVD versus with PVD, respectively. After adjustment with a multivariate Cox regression analysis, long-term all-cause survival was similar in patients with versus without PVD (hazard ratio, 1.16; 95% confidence interval, 0.69-1.93; P=.581). CONCLUSIONS: In contemporary PCI utilizing DESs, glycoprotein IIb/IIIa inhibitors, and clopidogrel, PVD is associated with a higher in-hospital and 4-year all-cause mortality. In our study, this difference in long-term survival was mainly driven by a higher rate of comorbidities in the PVD population that underwent PCI.

Impact of long-term statin therapy on postprocedural myocardial infarction in patients undergoing nonemergency percutaneous coronary intervention.

Periprocedural statin therapy has been shown to decrease the rate of myocardial infarctions (MIs) after percutaneous coronary intervention (PCI). However, the impact of long-term statin therapy on postprocedure MI remains unknown. We examined the impact of long-term statin therapy on cardiac enzyme (cardiac troponin I [cTnI] and creatine kinase-MB [CK-MB]) increases after PCI in patients undergoing nonemergency PCI. Using the 2004/2005 Cornell Angioplasty Registry, we evaluated 1,482 patients undergoing elective or urgent PCI with normal preprocedure cardiac enzymes levels (cTnI and CK-MB). The population was divided into 2 groups: (1) patients on long-term (≥7 days) statin therapy before PCI (n = 1,073) and (2) patients not on long-term statin regimen (n = 409). Cardiac enzyme levels after PCI were assessed at 8, 12, and 18 hours after PCI. An increase in cTnI ≥1 time upper-limit of normal (ULN) was observed in 830 patients (56.1%) and an increase in cTnI ≥3 times ULN was observed in 518 patients (35.0%). There was no difference in incidence of cTnI increases ≥3 times ULN in patients on long-term statin therapy versus those not on long-term statin therapy in the overall group (35.1% vs 34.5%, p = 0.855). There was a trend toward a lower incidence of small cTnI increases ≥1 time ULN in patients on long-term statin therapy versus those not receiving long-term statins (54.6% vs 59.7%, p = 0.090). Incidence of CK-MB increases ≥1 time or ≥3 times ULN and peak cTnI and CK-MB levels were similar between the 2 groups. In a subgroup of patients with unstable angina, long-term statin therapy decreased small cTnI increases (≥1 time ULN) after PCI (54.6% vs 64.3%, p = 0.023). The greatest benefit in decrease of MIs after PCI was seen in patients with unstable angina receiving long-term high-dose statin therapy. In conclusion, long-term statin therapy did not decrease the incidence of periprocedural MI in patients with stable coronary artery disease undergoing nonemergency PCI. In patients with unstable coronary syndromes, long-term statin therapy may be beneficial, particularly at a high dose.