Contemporary approach to cardiogenic shock care: a state-of-the-art review.

Cardiogenic shock (CS) is a time-sensitive and hemodynamically complex syndrome with a broad spectrum of etiologies and clinical presentations. Despite contemporary therapies, CS continues to maintain high morbidity and mortality ranging from 35 to 50%. More recently, burgeoning observational research in this field aimed at enhancing the early recognition and characterization of the shock state through standardized team-based protocols, comprehensive hemodynamic profiling, and tailored and selective utilization of temporary mechanical circulatory support devices has been associated with improved outcomes. In this narrative review, we discuss the pathophysiology of CS, novel phenotypes, evolving definitions and staging systems, currently available pharmacologic and device-based therapies, standardized, team-based management protocols, and regionalized systems-of-care aimed at improving shock outcomes. We also explore opportunities for fertile investigation through randomized and non-randomized studies to address the prevailing knowledge gaps that will be critical to improving long-term outcomes.

Effects of Escalating Temporary Mechanical Circulatory Support in Patients With Worsening Cardiogenic Shock.

BACKGROUND: Cardiogenic shock-related mortality is substantial, and temporary mechanical circulatory support (MCS) devices are frequently used. The authors aimed to describe patient characteristics and outcomes in patients with worsening cardiogenic shock requiring escalation of temporary MCS devices. METHODS: Worsening cardiogenic shock was defined as persistent hypotension, increasing doses of vasopressors/inotropes, worsening hypoperfusion, or worsening invasive hemo-dynamics. Escalation of temporary MCS devices was defined as adding or exchanging an existing MCS device. Variables were evaluated by logistic regression models and receiver operating characteristic curves. RESULTS: From July 1, 2016, to July 1, 2018, a total of 81 consecutive patients experienced worsening cardiogenic shock requiring temporary MCS escalation. The etiology of cardiogenic shock was heterogeneous (33.3% acute myocardial infarction and 61.7% decompen-sated heart failure). Younger age (<62 years), lower body mass index (<28.7 kg/m2), lower preescalation lactate levels (<3.1 mmol/L), higher postescalation blood pressure (>85 mm Hg), and lower postescalation lactate levels (<2.9 mmol/L) were associated with greater odds of survival. The presence of a pulmonary artery catheter at the time of escalation was associated with greater odds of survival (P = .05). Escalation of temporary MCS in Society for Cardiovascular Angiography and Interventions stage E shock was associated with 100% mortality (P = .05). The rate of overall survival to discharge was 32%. CONCLUSION: Patients requiring temporary MCS escalation represent a high-risk cohort. Further work is needed to improve outcomes in this patient population.

A Critical Review of Hemodynamically Guided Therapy for Cardiogenic Shock: Old Habits Die Hard.

PURPOSE OF REVIEW: Here, we review the importance of using hemodynamic data to guide therapy and risk stratification in cardiogenic shock as well as the various definitions of this syndrome that have been used in prior studies. Furthermore, we provide perspective regarding the controversy surrounding pulmonary artery (PA) catheter use as well as current society guidelines and scientific statements. Lastly, we review the technical aspects for accurate interpretation of data of cardiogenic shock. RECENT FINDINGS: More recent studies specifically evaluating cardiogenic shock patients have shown higher mortality when PA catheters were not used. Furthermore, initiatives are underway to develop more standardized definitions of cardiogenic shock, including the SCAI Shock Classification Scheme. Only by having a standardized fashion of conveying severity of shock will we be able to more systematically study this patient population and improve outcomes moving forward. SUMMARY: PA catheters are critical to the prognostication and management of a subset of patients with cardiopulmonary disease, particularly in those with pulmonary hypertension, cardiogenic shock, or requiring mechanical circulatory support or undergoing evaluation for advanced heart failure therapies.

Percutaneous Biventricular Hemodynamic Support Using Biatrial Extracorporeal Membrane Oxygenation.

We describe the use of a fully percutaneous, biatrial extracorporeal membrane oxygenation circuit, to provide biventricular support with left heart unloading by using a single TandemHeart (LivaNova, London, United Kingdom) circuit during high-risk percutaneous coronary intervention. (Level of Difficulty: Advanced.).

False-positive cerebrospinal fluid cryptococcus antigen in Libman-Sacks endocarditis.

BACKGROUND: Cryptococcus meningoencephalitis is a serious opportunistic infection associated with high morbidity and mortality in immunocompromised hosts, particularly patients with advanced AIDS disease. The diagnosis is established through cerebrospinal fluid (CSF) cryptococcus antigen detection and cultures. Cryptococcus antigen testing is usually the initial test of choice due its high sensitivity and specificity along with the quick availability of the results. CASE REPORT: We hereby report a case of a false-positive CSF cryptococcus antigen assay in a patient with systemic lupus erythematosus presenting with acute confusion. While initial CSF evaluation revealed a positive cryptococcus antigen assay, the patient's symptoms were inconsistent with cryptococcus meningoencephalitis. A repeat CSF evaluation, done 3 days later, revealed a negative CSF cryptococcus antigen assay. CONCLUSION: Given the patient's active lupus disease and the elevated antinuclear antibody titers, we believe that the initial positive result was a false positive caused by interference from autoantibodies.

Incorporating a Genetic Risk Score Into Coronary Heart Disease Risk Estimates: Effect on Low-Density Lipoprotein Cholesterol Levels (the MI-GENES Clinical Trial).

BACKGROUND: Whether knowledge of genetic risk for coronary heart disease (CHD) affects health-related outcomes is unknown. We investigated whether incorporating a genetic risk score (GRS) in CHD risk estimates lowers low-density lipoprotein cholesterol (LDL-C) levels. METHODS AND RESULTS: Participants (n=203, 45-65 years of age, at intermediate risk for CHD, and not on statins) were randomly assigned to receive their 10-year probability of CHD based either on a conventional risk score (CRS) or CRS + GRS ((+)GRS). Participants in the (+)GRS group were stratified as having high or average/low GRS. Risk was disclosed by a genetic counselor followed by shared decision making regarding statin therapy with a physician. We compared the primary end point of LDL-C levels at 6 months and assessed whether any differences were attributable to changes in dietary fat intake, physical activity levels, or statin use. Participants (mean age, 59.4±5 years; 48% men; mean 10-year CHD risk, 8.5±4.1%) were allocated to receive either CRS (n=100) or (+)GRS (n=103). At the end of the study period, the (+)GRS group had a lower LDL-C than the CRS group (96.5±32.7 versus 105.9±33.3 mg/dL; P=0.04). Participants with high GRS had lower LDL-C levels (92.3±32.9 mg/dL) than CRS participants (P=0.02) but not participants with low GRS (100.9±32.2 mg/dL; P=0.18). Statins were initiated more often in the (+)GRS group than in the CRS group (39% versus 22%, P<0.01). No significant differences in dietary fat intake and physical activity levels were noted. CONCLUSIONS: Disclosure of CHD risk estimates that incorporated genetic risk information led to lower LDL-C levels than disclosure of CHD risk based on conventional risk factors alone. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01936675.

Family history as a risk factor for peripheral arterial disease.

The association of a family history of peripheral arterial disease (PAD) with the presence of PAD is largely unknown. We conducted a case-control study of 2,296 patients with PAD (69 ± 10 years, 64% men) and 4,390 controls (66 ± 11 years, 62% men) identified from noninvasive vascular and stress testing laboratories at Mayo Clinic, Rochester, Minnesota, from October 2006 through June 2012. PAD was defined as an ankle brachial index of ≤ 0.9 at rest and/or after exercise, a history of lower extremity revascularization, or having poorly compressible leg arteries. Controls were patients with normal ankle brachial index or without a history of PAD. Family history of PAD was defined as having at least 1 first-degree relative who had undergone revascularization or stent placement for PAD before the age of 65 years. Logistic regression analyses were used to evaluate whether a family history of PAD was associated with the presence of PAD, independent of conventional risk factors. A family history of PAD was present more often in patients with PAD than in controls, with a resulting odds ratio (OR) of 2.20 (95% confidence interval [CI] 1.82 to 2.67). The association remained significant after adjustment for conventional risk factors (OR 1.97, 95% CI 1.60 to 2.42). The association was stronger in younger subjects (age <68 years; adjusted OR 2.46, 95% CI 1.79 to 3.38) than in older subjects (adjusted OR 1.61, 95% CI 1.22 to 2.12). A greater number of affected relatives with PAD was also associated with greater odds of presence of PAD (adjusted OR 1.86, 95% CI 1.48 to 2.33 and adjusted OR 2.56, 95% CI 1.60 to 4.11 for patients with 1 and ≥ 2 affected relatives with PAD, respectively). In conclusion, individuals with a family history of PAD have nearly double the odds of having PAD relative to those without such a history.

Family history as a risk factor for carotid artery stenosis.

BACKGROUND AND PURPOSE: We investigated whether family history of stroke or coronary heart disease (CHD) is associated with presence of carotid artery stenosis (CAS). METHODS: The study cohort included 864 patients (72±8 years; 68% men) with CAS and 1698 controls (61±11 years; 55% men) referred for noninvasive vascular testing. CAS was defined as ≥70% stenosis in the internal carotid artery on ultrasound or history of carotid revascularization. Controls did not have CAS or history of cerebrovascular disease or CHD. Family history of stroke and CHD was defined as having ≥1 first-degree relative who had stroke or CHD before age 65 years. Logistic regression analysis was used to evaluate whether family history of stroke or CHD was associated with presence of CAS, independent of conventional risk factors. RESULTS: Family history of stroke and CHD was present more often in patients with CAS than in controls, with a resulting odds ratios (95% confidence interval) of 2.02 (1.61-2.53) and 2.01 (1.70-2.37), respectively. The associations remained significant after adjustment for age, sex, body mass index, smoking, diabetes mellitus, hypertension, and dyslipidemia; odds ratios: 1.41 (1.06-1.90) and 1.69 (1.35-2.10), respectively. A greater number of affected relatives with stroke or CHD was associated with higher odds of CAS; adjusted odds ratios: 1.25 (0.91-1.72) and 1.46 (1.14-1.89) versus 2.65 (1.35-5.40) and 2.13 (1.57-2.90) for patients with 1 and ≥2 affected relatives with stroke and CHD, respectively. CONCLUSIONS: Family history of stroke, and of CHD were each associated with CAS, suggesting that shared genetic and environmental factors contribute to the risk of CAS. We show that (1) family history of stroke or CHD is independently associated with presence of CAS; (2) sibling history of stroke or CHD confers greater risk than parental history; and (3) the magnitude of the association is greater in those with greater number of affected relatives, independent of the size of the family [corrected].