Idiopathic Hypertrophic Subaortic Stenosis in the Elderly

Whiting, Richard B.; Powell, Wilson M.; Dinsmore, Robert E.; Sanders, Charles A.

doi:10.1056/nejm197107222850404

Cited by 73 publications

(13 citation statements)

References 14 publications

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“…10,11,23,24 In 1971, 32% of patients with idiopathic hypertrophic subaortic stenosis referred for catheterization at Massachusetts General Hospital were beyond their sixth decade. 25 Several studies of the natural history of elderly patients with hypertrophic cardiomyopathy suggested that, compared with earlier reports of alarming mortality rates, long-term prognosis in elderly patients is more favorable. 10,12,26 Total mortality rates and sudden death were significantly higher in younger patients with hypertrophic cardiomyopathy.…”

Section: Discussionmentioning

confidence: 99%

Sarcomere Protein Gene Mutations in Hypertrophic Cardiomyopathy of the Elderly

et al. 2002

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Background-Hypertrophic cardiomyopathy, a familial myocardial condition caused by sarcomere protein mutations, is usually recognized by early adulthood. Hypertrophic cardiomyopathy of the elderly has similar clinical features but, notably, a later age of onset and noncontributory family history. Causes of elderly-onset hypertrophic cardiomyopathy are unknown. Methods and Results-Eighteen women and 13 men diagnosed with late-onset hypertrophic cardiomyopathy were studied.Initial symptoms occurred at 59.

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Section: Discussionmentioning

confidence: 99%

Sarcomere Protein Gene Mutations in Hypertrophic Cardiomyopathy of the Elderly

et al. 2002

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“…6 Patients usually present with a heart murmur, dyspnea, angina, palpitations, or syncope. Syncope is the predominant "neurologic" complication of IHSS, and reflects ventricular outflow tract obstruction resulting in global brain hypoperfusion.…”

Section: Discussionmentioning

confidence: 99%

“…Some experimental studies published thus far use direct application of CCB to the cerebral vessels in vivo. 6 Other studies utilize a continuous intravascular infusion of CCB.…”

mentioning

confidence: 99%

“…The in vitro anticontractile effects of CCB on cerebral vessels appear particularly marked where receptor mediated agonists are the contractile agents. Yet studies of cerebral circulation which report no effect of CCB on resting diameter 6 or flow 3 -8 have not investigated the effects of CCB on receptor mediated constriction. Rather than agonists like serotonin, prostaglandin F^ or norepinephrine, hypocapnia or BaCl 2 have been used as the contractile stimulus.…”

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confidence: 99%

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Cerebrovascular complications associated with idiopathic hypertrophic subaortic stenosis.

Furlan¹,

Craciun²,

Raju

et al. 1984

Stroke

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One hundred fifty patients with idiopathic hypertrophic subaortic stenosis (IHSS) were followed-up for an average of 5.5 years. There were 95 males and 55 females with a mean age of 51 years. Patients usually presented with cardiac symptoms or syncope; no patient presented with stroke. Eight patients (5%) died during follow-up, all from cardiac causes. Eleven patients (7%) developed cerebrovascular complications; 5 (3%) had a stroke and 6 (4%) had TIA only. Patients with IHSS and atrial fibrillation have a much greater stroke risk. Mitral annulus calcification may also increase stroke risk in IHSS. However, stroke is almost never the presenting manifestation of IHSS, and the longterm risk of stroke for most patients with known IHSS is low.

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“…The lack of certainty that such patients have genetic HCM has led to alternative terminology such as sigmoid septum, USH, or (in the many such elderly patients with concomitant hypertension) hypertensive cardiomyopathy. 15,16 A characteristic feature of some cases of late-onset disease is increased angulation of the aorta with respect to the long axis of the LV. This may reflect a "functional" age-related change in cardiac shape that results in an upper septal bulge (sigmoid septum) and narrowing of the outflow tract.…”

Section: Discussionmentioning

confidence: 99%

Still a Kid at Heart

et al. 2011

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ForwardInformation about a real patient is presented in stages (boldface type) to an expert clinician (Dr Michael A. Fifer) , who responds to the information, sharing his reasoning with the reader (regular type). A Discussion by the authors follows.A 76-year-old man with a history of hypertrophic obstructive cardiomyopathy (HOCM), hypertension, dyslipidemia, and obstructive sleep apnea presents with dyspnea on exertion. This symptom has progressed slowly over the past year, to the point that he now has dyspnea on climbing 1 flight of stairs. The patient denies orthopnea, paroxysmal nocturnal dyspnea, edema, chest discomfort, palpitations, lightheadedness, and syncope. His medications are metoprolol, verapamil, disopyramide, rosuvastatin, and omeprazole. He is a retired electrician, is married with 3 adult children, and lives in Florida and Massachusetts, each for half the year. He has a history of heavy tobacco use but quit smoking more than 30 years ago. His family history is notable only for diabetes mellitus and stroke in his father; there are no family members with heart failure, hypertrophic cardiomyopathy (HCM), or sudden cardiac death (SCD).Dr Michael A. Fifer: This patient's presenting complaint is progressive dyspnea on exertion, for which he has possibly contributory comorbidities, namely, obstructive sleep apnea and hypertension. The history of HCM is particularly relevant because dyspnea is a common initial manifestation of the disease. 1 Dyspnea may occur in HCM as a result of a variety of mechanisms, including diastolic heart failure due to myocardial hypertrophy and fibrosis, left ventricular outflow tract (LVOT) obstruction, and associated mitral regurgitation (MR). Although the correlation between symptoms and the magnitude of the LVOT gradient is weak, 2 dyspnea is usually relieved by septal reduction therapy. In this patient, any or all of these factors might contribute to progressive dyspnea on exertion. More information regarding how the diagnosis of HOCM was made and how the condition has been managed since it was diagnosed would help determine whether it is primarily responsible for the worsening dyspnea.The diagnosis of HOCM was made 10 years before the current presentation. He presented then with exertional chest pain and dyspnea. An echocardiogram showed asymmetrical septal hypertrophy and a resting LVOT gradient. The diagnosis was confirmed by left-sided heart catheterization, which revealed an LVOT gradient that increased to 90 mm Hg with the Valsalva maneuver.Holter monitoring did not demonstrate ventricular tachycardia. The patient had substantial improvement in symptoms after undergoing medical therapy, which consisted of sustained-release metoprolol titrated up to 200 mg daily and sustained-release verapamil 120 mg daily. With the reappearance of dyspnea 1 year before the current presentation, disopyramide was added to the medical regimen, again with an initially favorable response. Dr Michael A. Fifer:Although HCM is classically diagnosed in young patients, the disease has a wide...

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Idiopathic Hypertrophic Subaortic Stenosis in the Elderly

Cited by 73 publications

References 14 publications

Sarcomere Protein Gene Mutations in Hypertrophic Cardiomyopathy of the Elderly

Sarcomere Protein Gene Mutations in Hypertrophic Cardiomyopathy of the Elderly

Cerebrovascular complications associated with idiopathic hypertrophic subaortic stenosis.

Still a Kid at Heart

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