The natural history, management, and outcome of takotsubo (stress) cardiomyopathy are incompletely understood. The International Takotsubo Registry, a consortium of 26 centers in Europe and the United States, was established to investigate clinical features, prognostic predictors, and outcome of takotsubo cardiomyopathy. Patients were compared with age- and sex-matched patients who had an acute coronary syndrome. Of 1750 patients with takotsubo cardiomyopathy, 89.8% were women (mean age, 66.8 years). Emotional triggers were not as common as physical triggers (27.7% vs. 36.0%), and 28.5% of patients had no evident trigger. Among patients with takotsubo cardiomyopathy, as compared with an acute coronary syndrome, rates of neurologic or psychiatric disorders were higher (55.8% vs. 25.7%) and the mean left ventricular ejection fraction was markedly lower (40.7±11.2% vs. 51.5±12.3%) (P<0.001 for both comparisons). Rates of severe in-hospital complications including shock and death were similar in the two groups (P=0.93). Physical triggers, acute neurologic or psychiatric diseases, high troponin levels, and a low ejection fraction on admission were independent predictors for in-hospital complications. During long-term follow-up, the rate of major adverse cardiac and cerebrovascular events was 9.9% per patient-year, and the rate of death was 5.6% per patient-year. Patients with takotsubo cardiomyopathy had a higher prevalence of neurologic or psychiatric disorders than did those with an acute coronary syndrome. This condition represents an acute heart failure syndrome with substantial morbidity and mortality. (Funded by the Mach-Gaensslen Foundation and others; ClinicalTrials.gov number, NCT01947621.)

Background—: The mechanisms by which the heart adapts to chronic pressure overload, producing compensated hypertrophy and eventually heart failure (HF), are still not well defined. We aimed to investigate the involvement of T cells in the progression to HF using a transverse aortic constriction (TAC) model. Methods and Results—: Chronic HF was associated with accumulation of T lymphocytes and activated/effector CD4 ⁺ T cells within cardiac tissue. After TAC, enlarged heart mediastinal draining lymph nodes showed a high density of both CD4 ⁺ and CD8 ⁺ T-cell subsets. To investigate the role of T cells in HF, TAC was performed on mice deficient for recombination activating gene 2 expression (RAG2KO) lacking B and T lymphocytes. Compared with wild-type TAC mice, RAG2KO mice did not develop cardiac dilation and showed improved contractile function and blunted adverse remodeling. Reconstitution of the T-cell compartment into RAG2KO mice before TAC enhanced contractile dysfunction, fibrosis, collagen accumulation, and cross-linking. To determine the involvement of a specific T-cell subset, we performed TAC on mice lacking CD4 ⁺ (MHCIIKO) and CD8 ⁺ T-cell subsets (CD8KO). In contrast to CD8KO mice, MHCIIKO mice did not develop ventricular dilation and dysfunction. MHCIIKO mice also displayed very low fibrosis, collagen accumulation, and cross-linking within cardiac tissue. Interestingly, mice with transgenic CD4 ⁺ T-cell receptor specific for ovalbumin failed to develop HF and adverse remodeling. Conclusions—: These results demonstrate for the first time a crucial role of CD4 ⁺ T cells and specific antigen recognition in the progression from compensated cardiac hypertrophy to HF.

Perioperative blood pressure management is a key factor of patient care for anesthetists, as perioperative hemodynamic instability is associated with cardiovascular complications. Hypertension is an independent predictive factor of cardiac adverse events in noncardiac surgery. Intraoperative hypotension is one of the most encountered factors associated with death related to anesthesia. In the preoperative setting, the majority of antihypertensive medications should be continued until surgery. Only renin-angiotensin system antagonists may be stopped. Hypertension, especially in the case of mild to moderate hypertension, is not a cause for delaying surgery. During the intraoperative period, anesthesia leads to hypotension. Hypotension episodes should be promptly treated by intravenous vasopressors, and according to their etiology. In the postoperative setting, hypertension predominates. Continuation of antihypertensive medications and postoperative care may be insufficient. In these cases, intravenous antihypertensive treatments are used to control blood pressure elevation.

Spinal anesthesia-induced hypotension (SAIH) occurs frequently, particularly in the elderly and in patients undergoing caesarean section. SAIH is caused by arterial and venous vasodilatation resulting from the sympathetic block along with a paradoxical activation of cardioinhibitory receptors. Bradycardia after spinal anesthesia (SA) must always be treated as a warning sign of an important hemodynamic compromise. Fluid preloading (before initiation of the SA) with colloids such as hydroxyethyl starch (HES) effectively reduces the incidence and severity of arterial hypotension, whereas crystalloid preloading is not indicated. Co-loading with crystalloid or colloid is as equally effective to HES preloading, provided that the speed of administration is adequate (ie, bolus over 5 to 10 minutes). Ephedrine has traditionally been considered the vasoconstrictor of choice, especially for use during SAIH associated with bradycardia. Phenylephrine, a α₁ adrenergic receptor agonist, is increasingly used to treat SAIH and its prophylactic administration (ie, immediately after intrathecal injection of local anesthetics) has been shown to decrease the incidence of arterial hypotension. The role of norepinephrine as a possible alternative to phenylephrine seems promising. Other drugs, such as serotonin receptor antagonists (ondansetron), have been shown to limit the blood pressure drop after SA by inhibiting the Bezold–Jarisch reflex (BJR), but further studies are needed before their widespread use can be recommended.

Background: Atrial fibrillation (AF) commonly affects patients with cardiac amyloidosis (CA). Amyloid deposition within the left atrium may be responsible for the subtype of AF in either permanent or non-permanent form. The prognostic implications of AF and its clinical subtype according to the type of CA are still controversial in this population. This study sought to investigate the prevalence, incidence and prognostic implications of AF and the clinical subtype of AF (permanent or non-permanent) in patients with CA. Methods: Two hundred and thirty-eight patients with CA and full medical records were retrospectively enrolled in the study: About 115 (48%) with light chain (AL) amyloidosis and 123 (52%) with transthyretin amyloidosis (ATTR). Patient’s medical records were reviewed to establish baseline prevalence, incidence and impact on all-cause and cardiovascular mortality during follow-up of AF. Results: One hundred and four (44%) patients had history of AF at the time of diagnosis: 62 (60%) permanent and 42 (40%) non-permanent. There were 30 (26%) and 74 (60%) patients with history of AF among patients with AL and ATTR (including 5 hereditary and 69 wild-type), respectively (p<.0001). During the follow-up, 48 new patients developed AF (29, 12 and 7 among patients with AL, wild-type ATTR and hereditary ATTR). After adjustment for age, survival was similar in patients with or without history of AF (HR 0.87 (95% CI, 0.60 to 1.27; p = .467). AF had no impact on cardiovascular mortality. Among the 152 patients with history of AF included in the whole study, there were 75 (49%) patients with permanent AF. After adjustment for age, survival was similar in patients with permanent and non-permanent AF: HR 1.29 (95% CI, 0.84 to 1.99; p = .251). The results were the same among patients with AL or wild-type amyloidosis. Subtype of AF had no impact on cardiovascular mortality. Conclusions: AF is common in patients with CA. However, AF and clinical subtype of AF have no impact on all-cause mortality, whatever the type of amyloidosis.