Occurrence and Frequency of Arrhythmias in Hypertrophic Cardiomyopathy in Relation to Delayed Enhancement on Cardiovascular Magnetic Resonance

Adabag, Selçuk; Maron, Barry J.; Appelbaum, Evan; Harrigan, Caitlin; Buros, Jacqueline L.; Gibson, C. Michael; Lesser, John R.; Hanna, Constance A.; Udelson, James E.; Manning, Warren J.; Maron, Martin S.

doi:10.1016/j.jacc.2007.11.071

Cited by 600 publications

(440 citation statements)

References 44 publications

(49 reference statements)

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“…It is an early manifestation of HCM even before hypertrophic remodeling 26. Meanwhile, myocardial fibrosis is a major determinant of SCD, ventricular tachyarrhythmia, left ventricular dysfunction, and heart failure 26, 27, 28. Our results showed that elevated hsCRP predicted an increased risk for adverse outcomes in patients with HCM.…”

Section: Discussionmentioning

confidence: 59%

Prognostic Significance of Plasma High‐Sensitivity C‐Reactive Protein in Patients With Hypertrophic Cardiomyopathy

Zhu

Zou

Wang

et al. 2017

JAHA

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BackgroundElevated high‐sensitivity C‐reactive protein (hsCRP) has been associated with increased risks of adverse outcomes of various cardiovascular diseases. The relationship between hsCRP and the prognosis of hypertrophic cardiomyopathy remains to be evaluated.Methods and ResultsThe study used an observational cohort methodology. A total of 490 patients were enrolled in the Fuwai Hospital from 2001 to 2011 and were followed for 3.7±2.0 years. According to the risk category of hsCRP, subjects in the high hsCRP group (>3.0 mg/L) had a higher risk of developing adverse events than the low hsCRP group (<1.0 mg/L): cardiovascular death (adjusted hazard ratios[HR] 5.41, 95% CI 1.96–14.93, P=0.001), all‐cause mortality (adjusted HR 4.78, 95% CI 1.99–11.47, P<0.001), sudden cardiac death (adjusted HR 11.29, 95% CI 1.38–92.20, P=0.024), and heart failure–related death (adjusted HR 4.38, 95% CI 1.15–16.60, P=0.030). Similarly, the continuous variable of hsCRP was also an independent predictor for adverse outcomes: cardiovascular death (adjusted HR 1.15, 95% CI 1.06–1.25, P=0.001), all‐cause mortality (adjusted HR 1.17, 95% CI 1.09–1.26, P<0.001), sudden cardiac death (adjusted HR 1.20, 95% CI 1.06–1.36, P=0.003), and heart failure–related death (adjusted HR 1.15, 95% CI 1.02–1.30, P=0.020).ConclusionsOur results indicate that elevated plasma hsCRP is associated with increased risk for adverse outcomes in patients with hypertrophic cardiomyopathy.

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Section: Discussionmentioning

confidence: 59%

Prognostic Significance of Plasma High‐Sensitivity C‐Reactive Protein in Patients With Hypertrophic Cardiomyopathy

Zhu

Zou

Wang

et al. 2017

JAHA

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“…S4, Table S1). An alternative possibility is that electrical uncoupling of CMs results from interstitial fibrosis and heterogeneous loss of connexin43 gap junctions (53)(54)(55). In this regard, IL-1␤-evoked COX-2 expression, depressed in CMs, was increased in fibroblasts harvested from CM-COX-2 KO hearts (Fig.…”

Section: Discussionmentioning

confidence: 98%

Cardiomyocyte cyclooxygenase-2 influences cardiac rhythm and function

Wang

Patel

Ricciotti

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

108

105

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Nonsteroidal anti-inflammatory drugs selective for inhibition of COX-2 increase heart failure and elevate blood pressure. The COX-2 gene was floxed and crossed into merCremer mice under the ␣-myosin heavy-chain promoter. Tamoxifen induced selective deletion of COX-2 in cardiomyocytes depressed cardiac output, and resulted in weight loss, diminished exercise tolerance, and enhanced susceptibility to induced arrhythmogenesis. The cardiac dysfunction subsequent to pressure overload recovered progressively in the knockouts coincident with increasing cardiomyocyte hypertrophy and interstitial and perivascular fibrosis. Inhibition of COX-2 in cardiomyocytes may contribute to heart failure in patients receiving nonsteroidal anti-inflammatory drugs specific for inhibition of COX-2.arrhythmia ͉ heart failure ͉ knockout ͉ NSAIDs ͉ fibrosis R andomized, placebo-controlled trials indicate that nonsteroidal antinflammatory drugs (NSAIDs) specific for inhibition of cyclooxygense (COX)-2 confer an increased risk of myocardial infarction and stroke (1-5), effects explicable by suppression of COX-2-derived products, such as prostacyclin (PGI 2 ) and prostaglandia E 2 (PGE 2 ) (6). While, the clinical spectrum of hazard is dominated by a predisposition to thrombosis, an additional feature has been congestive heart failure (1-4). NSAIDs may variably increase blood pressure (7): studies in rodents (8, 9) and a meta-analysis of clinical studies (10) suggest that this reflects inhibition of COX-2 and the specificity with which this is attained (11). Elevation of blood pressure by manipulation of the prostaglandin pathway is conditioned by genetic background in rodents (12). However, given this caveat, deletion or inhibition of COX-2 (8, 13) and deletion of the E prostanoid (EP)-2 receptor (14, 15) or the I-prostanoid receptor (IP) (16) for the COX-2 products, PGE 2 and PGI 2 respectively, may each result in hypertension. Indeed, deletion of the IP in these mice also results in cardiac hypertrophy and fibrosis, effects ameliorated by coincident deletion of the receptor for thromboxane A 2 , the TP, a maneuver that does not, alone, affect blood pressure (16). By contrast, inhibition or deletion of COX-1 attenuates the hypertensive response to infusion of angiotensin II (8) or treatment with a COX-2 inhibitor (13). Although placebo-controlled trials provide unequivocal evidence that COX-2-specific NSAIDs confer a cardiovascular hazard, the number of events within each trial are insufficient to permit analysis of covariates. Thus, it is unknown whether congestive heart failure on NSAIDs results solely from or is exacerbated by hypertension.Although suppression of COX-2-derived prostanoids is sufficient to explain the cardiovascular hazard conferred by purposedesigned and older NSAIDs specific for inhibition of COX-2 (17), there has been interest in the possibility that some or all of these effects might reflect ''off target'' effects. One such example was an overview-trial analysis interpreted to suggest that arrhythmia, cardiac arrest, ...

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“…86 A new superparamagnetic iron oxide probe conjugated to recombinant human annexin has demonstrated diffuse myocardial signal loss in rats treated with doxorubicin, suggestive of apoptosis by CMR. 87,88 Myocardial fibrosis detected as delayed enhancement (DE) by CMR has proven prognostic value in coronary heart disease, 89 and restrictive myocardial diseases including aortic stenosis, 90 hypertrophic cardiomyopathy, 91,92 and the infiltrative diseases of sarcoidosis 93 and amyloidosis. 94 CMR studies in larger populations of patients receiving potentially cardiotoxic agents are needed to see whether the presence of fibrosis detected by gadolinium enhancement identifies a cohort of patients more vulnerable to the cardiotoxic effects of chemotherapy, who may benefit from more frequent and long-term follow-up, and earlier treatment with ACE inhibitors and beta blockade to reduce the incidence and severity of chemotherapy-induced heart failure.…”

Section: Cardiac Magnetic Resonance Imagingmentioning

confidence: 99%

Traditional and novel methods to assess and prevent chemotherapy-related cardiac dysfunction noninvasively

Schwartz

Jain

Storozynsky

2013

Journal of Nuclear Cardiology

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The field of cardio-oncology is challenged to address an ever greater spectrum of cardiotoxicity associated with combination chemotherapy, greater dose intensity, extremes of age, and enhanced patient survival which exposes more protracted risk of developing congestive heart failure (CHF). Recent reports of chemotherapy-induced hypertension as a common adverse effect of angiogenesis inhibitors and immunosuppressants clarify the need for routine blood pressure (BP) monitoring and guideline-based management of hypertension as an integral strategy to preserve LV function. Serial monitoring of radionuclide left ventricular ejection fraction (LVEF) in adults and echocardiography in children continues to provide outcome based, cost-effective prevention of CHF in high risk patients receiving chemotherapy. To optimize treatment and monitoring strategies to eliminate late-onset LV dysfunction and CHF, traditional and novel candidate methods for assessment of chemotherapy-induced LV dysfunction are reviewed. These include serial assessment of LV volume indices by gated SPECT ERNA and gated SPECT MPI, 3D echocardiography and contrast 2D echocardiography; longitudinal strain imaging, diastolic functional parameters, 123 I-MIBG, 111 In-Antimyosin antibody imaging, and 99m Tc-Annexin V apoptosis imaging, biomarkers including troponins and BNP; genetic markers, and both functional and tissue characterization techniques with T1 weighted and T2 weighted images with cardiac magnetic resonance imaging (CMR). In our quest to optimize strategies for long-term cancer survival and prevention of CHF for patients receiving chemotherapy, rigorous modality and guideline-specific clinical outcome trials are required. A new multi-modality monitoring approach is proposed, which integrates evidencebased strengths of CMR, echocardiography, ERNA, biomarkers, and BP management for surveillance and validation of cardiotoxicity and prevention of clinical heart failure in patients receiving a broad spectrum of cancer therapies.

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Occurrence and Frequency of Arrhythmias in Hypertrophic Cardiomyopathy in Relation to Delayed Enhancement on Cardiovascular Magnetic Resonance

Cited by 600 publications

References 44 publications

Prognostic Significance of Plasma High‐Sensitivity C‐Reactive Protein in Patients With Hypertrophic Cardiomyopathy

Prognostic Significance of Plasma High‐Sensitivity C‐Reactive Protein in Patients With Hypertrophic Cardiomyopathy

Cardiomyocyte cyclooxygenase-2 influences cardiac rhythm and function

Traditional and novel methods to assess and prevent chemotherapy-related cardiac dysfunction noninvasively

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