Carcinoid Crisis-Induced Acute Systolic Heart Failure.
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ABSTRACT:
SUBMITTER: Maddali MV
PROVIDER: S-EPMC8299771 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BACKGROUND:Post-systolic shortening (PSS) is a novel echocardiographic marker of myocardial dysfunction. Our objective was to assess the prognostic value of PSS in patients following acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI). METHODS:A total of 428 patients hospitalized for ACS (mean age 64?±?12?years, male 73%) underwent speckle tracking echocardiography following treatment with PCI (median 2?days). The individual endpoints were heart failure (HF), myocardial infarction (MI) and all-cause death. We excluded known HF. Presence of PSS was defined as post-systolic displacement ?20% of maximum strain in one cardiac cycle. The post-systolic index (PSI) was defined as (100?×?[maximum-strain cardiac cycle?-?peak-systolic strain])/(maximum-strain cardiac cycle)]. RESULTS:During median follow-up of 3.7?years (IQR 0.3, 5.2), 155 patients (36%) experienced HF, 52 (12%) had MI and 87 (20%) died from all causes. Patients experiencing HF had more walls displaying PSS (3.2 vs. 1.9 walls) and higher PSI (22% vs. 12%) (P?<?0.001 both). In Cox proportional hazards models adjusted for baseline characteristics, invasive and echocardiographic measurements, the risk of HF increased incrementally with increasing number of walls with PSS (HR 1.28 95%CI 1.12-1.46, P?<?0.001 per 1 increase in walls with PSS). The PSI remained an independent predictor of HF after adjustment (HR 1.61 95%CI 1.21-2.12, P?=?0.001 per 1% increase). In the same adjusted models, MI and all-cause death were not significantly associated with PSS. CONCLUSION:Presence of PSS provides novel and independent prognostic information regarding the risk of future HF in patients with ACS following PCI.
| S-EPMC6365100 | biostudies-literature
Project description:Introduction and importanceCarcinoid tumors are rare malignancies of neuroendocrine origin that can manifest with a constellation of systemic symptoms including right-sided cardiac involvement. Many patients with carcinoid heart disease require valve replacement, but intraoperative management of carcinoid syndrome varies within the literature.Case presentationA 72-year-old man with carcinoid syndrome underwent tricuspid and pulmonic valve replacement with multiple episodes of carcinoid crisis intraoperatively as well as right ventricular dysfunction after cardiopulmonary bypass.Clinical discussionOctreotide is the mainstay in prevention and treatment of intraoperative carcinoid crisis, but reported dosages and timing varies significantly. The use of exogenous catecholamines is also controversial as they are thought to paradoxically worsen carcinoid symptoms. Our patient was managed successfully with both an octreotide infusion and intermittent boluses, as well as exogenous catecholamines for right ventricular support during and after cardiopulmonary bypass.ConclusionThe management of carcinoid syndrome in patients undergoing valve surgery for carcinoid heart disease is dependent on timely prevention and treatment of carcinoid crisis and effective mitigation of right ventricular dysfunction.
| S-EPMC9829749 | biostudies-literature
Project description:BackgroundGuidelines recommend targeting decongestion in management of decompensated HF, with lower extremity edema often serving as the clinical target. LECW are seldom used in the acute setting, with a paucity of data on efficacy in HF, despite serving as a cornerstone of chronic lymphedema management.Primary objectiveStudy the efficacy and safety of LECW in acute decompensated HF.MethodsOpen-label, randomized, parallel-group clinical trial.Primary outcomesDays on intravenous (IV) diuretic therapy, total hospital length of stay (LOS), and 30-day all-cause readmission.Results32 patients were enrolled, with 29 patients completing the study. Enrollment was suspended due to the COVID-19 pandemic. Overall LOS was shorter in the intervention group (3.5 vs 6 days, p = 0.05), with no significant difference in total days on IV diuresis or 30-day readmission rate with use of LECW. Fewer patients required continuous diuretic infusion after treatment with LECW (0 vs 7 patients, p = 0.027). The intervention group scored significantly better on the MLWHF (55.5 vs 65, p = 0.021), including both the physical and emotional dimension scores. No adverse events were reported with use of LECW, including a significantly lower incidence of AKI (1 vs 13 patients, p = 0.005).ConclusionThe use of LECW resulted in reduced hospital LOS compared to standard therapy, with no difference in days of IV diuresis administration or 30-day readmission. Treatment with LECW also resulted in less continuous IV diuretic therapy, fewer incidence of AKI, and improved quality of life. Trends toward less escalation of diuresis, and greater reduction in edema were also observed.
| S-EPMC10432693 | biostudies-literature
Project description:Double-stranded RNA-dependent protein kinase (PKR) is a eukaryotic initiation factor 2? kinase that inhibits mRNA translation under stress conditions. PKR also mediates inflammatory and apoptotic signaling independently of translational regulation. Congestive heart failure is associated with cardiomyocyte hypertrophy, inflammation, and apoptosis, but the role of PKR in left ventricular hypertrophy and the development of congestive heart failure has not been examined.We observed increased myocardial PKR expression and translocation of PKR into the nucleus in humans and mice with congestive heart failure. To determine the impact of PKR on the development of congestive heart failure, PKR knockout and wild-type mice were exposed to pressure overload produced by transverse aortic constriction. Although heart size increased similarly in wild-type and PKR knockout mice after transverse aortic constriction, PKR knockout mice exhibited very little pulmonary congestion, well-preserved left ventricular ejection fraction and contractility, and significantly less myocardial fibrosis compared with wild-type mice. Bone marrow-derived cells from wild-type mice did not abolish the cardiac protective effect observed in PKR knockout mice, whereas bone marrow-derived cells from PKR knockout mice had no cardiac protective effect in wild-type mice. Mechanistically, PKR knockout attenuated transverse aortic constriction-induced tumor necrosis factor-? expression and leukocyte infiltration and lowered cardiac expression of proapoptotic factors (Bax and caspase-3), so that PKR knockout hearts were more resistant to transverse aortic constriction-induced cardiomyocyte apoptosis. PKR depletion in isolated cardiomyocytes also conferred protection against tumor necrosis factor-?- or lipopolysaccharide-induced apoptosis.PKR is a maladaptive factor upregulated in hemodynamic overload that contributes to myocardial inflammation, cardiomyocyte apoptosis, and the development of congestive heart failure.
| S-EPMC3972332 | biostudies-literature
Project description:BackgroundRenin-angiotensin-system blockers (RASB) improve clinical outcomes in patients with chronic heart failure with reduced fraction; however, there remains ambiguity whether RASB therapy should be continued during the treatment of acute decompensated heart failure (ADHF).HypothesisIn comparison to patients with RASB use, RASB discontinuation in ADHF will be associated with worsening renal function, hypotension, and adverse long-term clinical outcomes.MethodsPatients in the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization (ESCAPE) trial were separated into four groups based on RASB use at baseline and discharge: continuation (n = 316), discontinuation (n = 21), initiation (n = 42), and nonuse (n = 23). Post-discharge outcomes were validated in an independent ADHF cohort admitted to the Cleveland Clinic (n = 253).ResultsRASB discontinuation and nonuse were associated with higher serial creatinine and blood urea nitrogen levels than RASB continuation or initiation (P <?.001 for both), but not with serial potassium and systolic blood pressure measurements. No other clinical parameter changes were significant. In comparison to RASB continuation, RASB discontinuation and nonuse was associated with ~75% increased risk of a 180-day composite of death, transplant, or rehospitalization (HR 1.87, 95% CI 1.09-3.20, P =?0.02 and HR 1.72, CI 1.04-2.82, P =?.03, respectively). Post-discharge outcomes were similar in the validation cohort.ConclusionCompared to RASB continuation, RASB discontinuation and nonuse were associated with higher baseline and serial creatinine levels during treatment for ADHF, but not with changes in SBP and potassium levels. Furthermore, RASB discontinuation and nonuse in ADHF were associated with an increased risk of adverse clinical outcomes.
| S-EPMC6788475 | biostudies-literature
Project description:Screening for systolic heart failure (SHF) has been problematic. Heart failure management guidelines suggest screening for structural heart disease and SHF prevention strategies should be a top priority. We developed a multi-protein biomarker panel using saliva as a diagnostic medium to discriminate SHF patients and healthy controls. We collected saliva samples from healthy controls (n = 88) and from SHF patients (n = 100). We developed enzyme linked immunosorbent assays to quantify three specific proteins/peptide (Kallikrein-1, Protein S100-A7, and Cathelicidin antimicrobial peptide) in saliva samples. The analytical and clinical performances and predictive value of the proteins were evaluated. The analytical performances of the immunoassays were all within acceptable analytical ranges. The multi-protein panel was able to significantly (p < 0.001) discriminate saliva samples collected from patients with SHF from controls. The multi-protein panel demonstrated good performance with an overall diagnostic accuracy of 81.6% (sensitivity of 79.2% and specificity of 85.7%) when distinguishing SHF patients from healthy individuals. In conclusion, we have developed immunoassays to measure the salivary concentrations of three proteins combined as a panel to accurately distinguish SHF patients from healthy controls. While this requires confirmation in larger cohorts, our findings suggest that this three-protein panel has the potential to be used as a biomarker for early detection of SHF.
| S-EPMC6995570 | biostudies-literature
Project description:Inducible nitric oxide synthase (iNOS) protein is expressed in cardiac myocytes of patients and experimental animals with congestive heart failure (CHF). Here we show that iNOS expression plays a role in pressure overload-induced myocardial chamber dilation and hypertrophy. In wild-type mice, chronic transverse aortic constriction (TAC) resulted in myocardial iNOS expression, cardiac hypertrophy, ventricular dilation and dysfunction, and fibrosis, whereas iNOS-deficient mice displayed much less hypertrophy, dilation, fibrosis, and dysfunction. Consistent with these findings, TAC resulted in marked increases of myocardial atrial natriuretic peptide 4-hydroxy-2-nonenal (a marker of lipid peroxidation) and nitrotyrosine (a marker for peroxynitrite) in wild-type mice but not in iNOS-deficient mice. In response to TAC, myocardial endothelial NO synthase and iNOS was expressed as both monomer and dimer in wild-type mice, and this was associated with increased reactive oxygen species production, suggesting that iNOS monomer was a source for the increased oxidative stress. Moreover, systolic overload-induced Akt, mammalian target of rapamycin, and ribosomal protein S6 activation was significantly attenuated in iNOS-deficient mice. Furthermore, selective iNOS inhibition with 1400W (6 mg/kg per hour) significantly attenuated TAC induced myocardial hypertrophy and pulmonary congestion. These data implicate iNOS in the maladaptative response to systolic overload and suggest that selective iNOS inhibition or attenuation of iNOS monomer content might be effective for treatment of systolic overload-induced cardiac dysfunction.
| S-EPMC2386857 | biostudies-literature
Project description:Background: Acute effects of positive airway pressure (PAP) [including continuous PAP (CPAP) and adaptive servo-ventilation, an advanced form of bi-level PAP] on functional mitral regurgitation (fMR) in patients with heart failure (HF) with left ventricular (LV) systolic dysfunction remain unclear. Thus, whether PAP therapy reduces fMR in such patients with HF was investigated. Methods and Results: Twenty patients with HF and LV systolic dysfunction defined as LV ejection fraction (LVEF) <50% (14 men; mean LVEF, 35.0 ± 11.5%) with fMR underwent echocardiography during 10-min CPAP (4 and 8 cm H2O) and adaptive servo-ventilation. For fMR assessment, MR jet area fraction, defined as the ratio of MR jet on color Doppler to the left atrial area, was measured. The forward stroke volume (SV) index (fSVI) was calculated from the time-velocity integral, cross-sectional area of the aortic annulus, and body surface area. fMR significantly reduced on CPAP at 8 cm H2O (0.30 ± 0.12) and adaptive servo-ventilation (0.29 ± 0.12), compared with the baseline phase (0.37 ± 0.12) and CPAP at 4 cm H2O (0.34 ± 0.12) (P < 0.001). The fSVI did not change in any of the PAP sessions (P = 0.888). However, significant differences in fSVI responses to PAP were found between sexes (P for interaction, 0.006), with a significant reduction in fSVI in women (P = 0.041) and between patients with baseline fSVI ? and < the median value (27.8 ml/m2, P for interaction, 0.018), with a significant fSVI reduction in patients with high baseline fSVI (P = 0.028). In addition, significant differences were found in fSVI responses to PAP between patients with LV end-systolic volume (LVESV) index ? and < the median value (62.0 ml/m2, P for interaction, 0.034), with a significant fSVI increase in patients with a high LVESV index (P = 0.023). Conclusion: In patients with HF, LV systolic dysfunction, and fMR, PAP can alleviate fMR without any overall changes in forward SV. However, MR alleviation due to PAP might be associated with a decrease in forward SV in women with high baseline SV, whereas MR alleviation due to PAP might be accompanied by increased forward SV in patients with a dilated LV.
| S-EPMC5703848 | biostudies-literature
Project description:Activation of AMP-activated protein kinase (AMPK)-?2 protects the heart against pressure overload-induced heart failure in mice. Although metformin is a known activator of AMPK, it is unclear whether its cardioprotection acts independently of an AMPK?2-dependent pathway. Because the role of AMPK?1 stimulation on remodeling of failing hearts is poorly defined, we first studied the effects of disruption of both the AMPK?1 and AMPK?2 genes on the response to transverse aortic constriction-induced left ventricular (LV) hypertrophy and dysfunction in mice. AMPK?2 gene knockout significantly exacerbated the degree of transverse aortic constriction-induced LV hypertrophy and dysfunction, whereas AMPK?1 gene knockout had no effect on the degree of transverse aortic constriction-induced LV hypertrophy and dysfunction. Administration of metformin was equally effective in attenuating transverse aortic constriction-induced LV remodeling in both wild-type and AMPK?2 knockout mice, as evidenced by reduced LV and lung weights, a preserved LV ejection fraction, and reduced phosphorylation of mammalian target of rapamycin (p-mTOR(Ser2448)) and its downstream target p-p70S6K(Thr389). These data support the notion that activation of AMPK?1 plays a negligible role in protecting the heart against the adverse effects of chronic pressure overload, and that metformin protects against adverse remodeling through a pathway that seems independent of AMPK?2.
| S-EPMC4026291 | biostudies-literature
Project description:Acute heart failure (AHF) is a life-threatening emergency, which largely profits from early diagnosis and treatment. The prevalence of AHF is difficult to assess, estimates range between 1 and 12% in the general population. Despite recent therapeutic advances, in-hospital mortality is high with estimates varying from 4 and 18% in different registries. Due to large differences in AHF definitions and selection criteria AHF populations vary in their characteristics and outcomes. This is especially true for randomized clinical trials and the external validity of some of these trials is questionable. Additionally, the timing of data collection and/or initiation of new therapies vary with the setting of trials. The aim of this article is to call attention to the difference in AHF populations and to emphasize the need for research to clearly define these populations. AHF populations from registries and clinical trials are the basis for evidence-based management strategies. It is important that these populations represent the patients in whom these strategies will be applied in routine care.
| S-EPMC5074292 | biostudies-literature