Impaired Peripheral Vasoconstriction in Response to Alpha-Adrenergic Stimulation in Patients With Idiopathic Hypertrophic Cardiomyopathy

Kawano, Satoru; Iida, Keiji; Nishi, Isao; Iwasaki, Yuko; Masumi, Tomoko; Sugishita, Yasuro; Yamaguchi, Iwao

doi:10.1253/jcj.62.903

Cited by 6 publications

(4 citation statements)

References 24 publications

(16 reference statements)

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“…It is possible that the profuse hypotension and refractoriness to phenylephrine could be related to the impaired baroreflex sensitivity and alpha‐adrenergic receptor mediated vasoconstriction that have been reported in some patients with HCM 16,17 …”

Section: Discussionmentioning

confidence: 99%

“…It is possible that the profuse hypotension and refractoriness to phenylephrine could be related to the impaired baroreflex sensitivity and alphaadrenergic receptor mediated vasoconstriction that have been reported in some patients with HCM. 16,17 Myectomy is preferred over mitral replacement for relief of LV outflow tract obstruction in HCM patients refractory to pharmacotherapy; at our institution myectomy is performed with a ratio of >10:1 in obstructive HCM patients. In these two patients it was our preoperative judgment that they would be best served by having a mitral valve replacement: (1) they had only mild septal thickening, 17 mm and 16 mm, respectively.…”

Section: Discussionmentioning

confidence: 99%

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Reversal of Acute Systolic Dysfunction and Cardiogenic Shock in Hypertrophic Cardiomyopathy by Surgical Relief of Obstruction

Sherrid¹,

Balaran

Korzeniecki³

et al. 2011

Echocardiography

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A 70-year-old male with known hypertrophic cardiomyopathy (HCM) and latent obstruction presented with new onset of cardiogenic shock. He had a new resting left ventricular (LV) outflow gradient of 90 mmHg, and new severe LV systolic dysfunction. Because of rapid deterioration despite medical management he was urgently sent for surgical relief of obstruction, which immediately reversed both the LV dysfunction and shock. A second patient, a 58-year-old male also with hypertrophic cardiomyopathy and latent obstruction presented with collapse, cardiogenic shock, 135 mmHg resting LV outflow gradient and new severe LV systolic dysfunction. His profound shock was irreversible with pharmacologic management, but surgical relief of obstruction reversed both his LV dysfunction and shock. Echocardiography plays a pivotal role in the management of these acutely ill patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Reversal of Acute Systolic Dysfunction and Cardiogenic Shock in Hypertrophic Cardiomyopathy by Surgical Relief of Obstruction

Sherrid¹,

Balaran

Korzeniecki³

et al. 2011

Echocardiography

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“…The vasopressor support, initially with dopamine and later with noradrenaline, was correct from a physiopathological point of view, although the literature recommends the use of phenylephrine 54 . The IV administration of beta-blockers and disopyramide 38 are other treatment options.…”

Section: Clinical Aspectsmentioning

confidence: 99%

Caso 01/2008: paciente jovem do sexo feminino, portadora de forma familiar de cardiomiopatia hipertrófica que evoluiu com síncopes, arritmia ventricular complexa e choque cardiogênico

Harada¹,

Morita²,

Arteaga³

et al. 2008

Arq. Bras. Cardiol.

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A 19-year-old female patient with the diagnosis of hypertrophic cardiomyopathy was referred to the hospital (Heart Institute (InCor), University of São Paulo Medical School, Brazil) for treatment.The diagnosis of hypertrophic cardiomyopathy had been achieved at 5 years of age at the time of the cardiologic assessment carried out in the patient's family. The assessment was indicated considering the family history of several cases of the disease. The patient's father had a diagnosis of hypertrophic cardiomyopathy, which evolved to cardiac dilation and he was finally submitted to orthotopic heart transplant. Paternal uncles and grandparents also presented the disease. Two of the patient's brothers presented the same condition and one had died of sudden death.The patient presented repeated episodes of syncope during the clinical evolution. She had been submitted to the implantation of an implantable cardiodefibrillator (ICD) three years before. After the implant, she started to present syncope episodes again and no defibrillating activity could be detected in the implanted device. She was then referred to Instituto do Coração (InCor).At the first medical assessment at the hospital (11/16/2006), she complained of frequent episodes of palpitation associated to short-term general malaise, precordial pain, shortness of breath and pre-syncope. The last syncope episode had occurred four months prior to this medical visit. She also complained about shortness of breath triggered by strenuous physical effort.The patient did not use beta-blockers or calcium channel antagonists. These drugs had been previously prescribed and used by the patient, but they had caused arterial hypotension and consequently, their use was withdrawn. , regular pulse, heart rate = 60 bpm and BP=100 / 60 mmHg. Lung assessment was normal. The heart assessment showed systolic murmur at aortic focus +++/6 irradiating to the left sternum border and mitral area.The electrocardiogram (11/13/2006) disclosed pacemaker rhythm, normofunctioning double chamber and left atrial overload.Laboratory assessment (11/13/2006) showed hemoglobin = 13.6 g/dl, hematocrit = 41%, creatinine = 1.02 mg/dl, potassium = 4.6 mEq/l and sodium = 139 mEq/l.The echocardiogram (11/28/2006) showed an aortic diameter of 24 mm, left atrium diameter of 44 mm, diastolic and systolic left ventricle diameters of 34 and 22 mm, respectively, with a left ventricle ejection fraction of 66%; the interventricular septum thickness was 18 mm and the left ventricular posterior wall thickness was 9 mm. There was a marked asymmetric hypertrophy of the septal and lateral walls with a hyperdynamic systolic performance, no alterations in segmental mobility, mild diastolic dysfunction, mild mitral insufficiency and maximum intra-ventricular gradient of 27 mmHg at rest.Holter monitoring of the cardiac rhythm (11/27/2006) disclosed a sinus rhythm, alternating with the rhythm stimulated by the artificial pacemaker. The atrioventricular conduction alternated periods of normal conduction with others that presen...

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“…Disturbed endothelial function in patients with coronary artery disease stimulates vasoconstriction, smooth muscle migration and proliferation, increased lipid deposition in the vessel wall and possibly coronary thrombosis, thereby promoting myocardial ischemia, which may further contribute directly or indirectly to the progression of LV dysfunction [79,80]. It is well established that functional vascular reactivity is altered in heart failure, limiting peripheral blood flow to exercising skeletal muscle and subsequently reducing physical exercise tolerance [81] ( fig.…”

Section: Endothelial Markersmentioning

confidence: 99%

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Serebruany¹,

Davis

Meister

et al. 2001

Heart Drug

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Knowledge of the pathogenesis of congestive heart failure (CHF) has improved greatly in recent years. Nevertheless, this disease still causes high morbidity and mortality in the Western world. In particular, there have been many advancements in our understanding, treatment and prophylaxis of CHF in recent years, yet the incidence of this disease continues to rise. Due to the staggering numbers of patients afflicted, CHF is becoming the most expensive burden on the health care system. The relationship between the deterioration of cardiac function and ongoing ischemic events has not been fully investigated and could conceivably be both monitored and modulated via various biomarkers. Recent data also indicate that heart failure is associated with altered hemostasis, i.e. a prothrombotic state which can lead to complications arising from occlusive and/or thromboembolic phenomena. Although the incidence of overt and clinically apparent thrombotic events is low, it is possible that subclinical events contribute to the increasing morbidity and mortality from this disease. These subclinical events may include silent ischemic events or microinfarcts which are being recognized as contributing to the progression of heart failure. As far as nonpharmacologic approaches to heart failure are concerned, the use of uniform exercise training regimens in heart failure is still a very controversial topic. Before more definitive recommendations can be made regarding the justification of such procedures, further large-scale studies investigating the effects of physical exercise on the development and progression of heart failure are needed. Furthermore, these studies must have sufficient statistical power to detect effects on clinical outcomes, specifically mortality. The purpose of this review article is to bridge the gap between biomarkers, exercise training and heart failure by discussing our current knowledge of different markers of platelet activation, thrombin generation, inflammation, endothelial dysfunction and myocardial necrosis in CHF patients undertaking physical exercise.

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Impaired Peripheral Vasoconstriction in Response to Alpha-Adrenergic Stimulation in Patients With Idiopathic Hypertrophic Cardiomyopathy

Cited by 6 publications

References 24 publications

Reversal of Acute Systolic Dysfunction and Cardiogenic Shock in Hypertrophic Cardiomyopathy by Surgical Relief of Obstruction

Reversal of Acute Systolic Dysfunction and Cardiogenic Shock in Hypertrophic Cardiomyopathy by Surgical Relief of Obstruction

Caso 01/2008: paciente jovem do sexo feminino, portadora de forma familiar de cardiomiopatia hipertrófica que evoluiu com síncopes, arritmia ventricular complexa e choque cardiogênico

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

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