Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy: randomised double-blind controlled trial

Malik, Rayaz A.; Williamson, Sheila; Abbott, Caroline A.; Carrington, Anne L.; Iqbal, Jawaid; Schady, W.; Boulton, Andrew J.M.

doi:10.1016/s0140-6736(98)02478-7

Cited by 267 publications

(148 citation statements)

References 26 publications

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“…After 12 months, improvement of CAN was observed in patients treated both with quinapril or losartan, while their combination was slightly even more effective [48]. Beneficial effect of quinapril on CAN has also been observed in another study [49], while no significant changes in CAN was detected after 12 months treatment with trandolapril [50].…”

Section: Discussionmentioning

confidence: 72%

Why Not to Use the Handgrip Test in the Assessment of Cardiovascular Autonomic Neuropathy Among Patients with Diabetes Mellitus?

Körei

Kempler

Istenes

et al. 2016

CVP

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Section: Discussionmentioning

confidence: 72%

Why Not to Use the Handgrip Test in the Assessment of Cardiovascular Autonomic Neuropathy Among Patients with Diabetes Mellitus?

Körei

Kempler

Istenes

et al. 2016

CVP

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“…Gottlieb et al noted that post-myocardial infarction diabetic patients had a 36% reduction in mortality with the use of beta-blockers ( 19 ). Th e use of angiotensin-converting enzyme inhibitors hinders downstream sympathetic outfl ow; 1-year use of quinapril resulted in some benefi t for treating CAN ( 20 ), while a year of trandolapril resulted in no benefi ts of autonomic function or neuropathy symptoms in patients with CAN ( 21 ). Diabetic patients with neuropathy were treated for a year with an aldose reductase inhibitor (zopolrestat) and showed improved resting and exercise left ventricular ejection fractions, cardiac output, and stroke volume ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Autonomic Neuropathy

McCarty

Silverman

2016

Baylor University Medical Center Proceedings

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Cardiovascular autonomic neuropathy often goes unrecognized. We present a case of a 22-year-old man with multiple manifestations of this disease, including weakness, dizziness, fatigue, tachycardia, abnormal QTc, and orthostasis, which occurred 2 years after his type 1 diabetes diagnosis. He exhibited parasympathetic denervation with resting tachycardia and exercise intolerance but also had evidence of orthostatic hypotension, which suggests sympathetic denervation. He did not have complete cardiovascular autonomic reflex testing, which would have been helpful, but improved with aggressive diabetes treatment and the increase of beta-blockade. It is important to identify these patients to understand their signs and symptoms and consider appropriate therapies. C ardiovascular autonomic neuropathy (CAN) is a serious and common complication of diabetes mellitus (DM) that is often not recognized. Diabetes mellitus aff ects more than 26 million people in the United States. Prevalence rates of CAN increase with age and duration of DM. Th e Diabetes Control and Complication Trial reported rates as high as 35% in type 1 DM and 44% in type 2 DM, with a prevalence rate of up to 60% in longstanding diabetics ( 1 ). Th e presence of CAN is associated with increased cardiovascular mortality and is the cause of cardiac dysfunction and multiple clinical symptoms, including resting tachycardia, exercise intolerance, postural hypotension, silent ischemia, cardiomyopathy, and perioperative instability ( 1 -4 ). CASE REPORTA 22-year-old African American man with a 2-year history of type 1 DM presented to the clinic with complaints of fatigue, decreased exercise tolerance, palpitations, and persistent tachycardia. He was 6' tall and 147 lb. His blood pressure and heart rate recorded supine, sitting, and standing after 3 minutes were 138/80 mm Hg/105 beats per minute (bpm), 130/88 mm Hg/122 bpm, and 98/72 mm Hg/126 bpm, respectively. His exam revealed the presence of peripheral neuropathy with numbness and tingling extending bilaterally to the shin. A Holter monitor recorded a marked decrease in his heart rate variability (HRV), with HRV of 20 bpm over each hour and an average of 118 bpm with no dipping during sleep. His thyroid function was normal. An electrocardiogram exhibited sinus

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“…70 In studies of human diabetes, two small clinical trials demonstrated that diabetic neuropathy was improved by treatment of patients with trandolapril or lisinopril. 71,72 Diabetes causes impairment in vascular relaxation in response to acetylcholine and calcitonin gene-related peptide in epineurial arterioles of the sciatic nerve. 73,74 Acetylcholine-induced vascular relaxation is endothelium dependent and mediated by NO and endothelium-derived hyperpolarizing factor, and both are impaired by diabetes.…”

Section: Diabetic Neuropathymentioning

confidence: 99%

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

2009

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Since their inception, angiotensin-converting enzyme (ACE) inhibitors have been used as first-line therapy for the treatment of cardiovascular and renal diseases. They restore the balance between the vasoconstrictive salt-retentive and hypertrophy-causing peptide angiotensin II (Ang II) and bradykinin, a vasodilatory and natriuretic peptide. As ACE is a promiscuous enzyme, ACE inhibitors alter the metabolism of a number of other vasoactive substances. ACE inhibitors decrease systemic vascular resistance without increasing heart rate and promote natriuresis. They have been proven effective in the treatment of hypertension, and reduce mortality in congestive heart failure and left ventricular dysfunction after myocardial infarction. They inhibit ischemic events and stabilize plaques. Furthermore, they delay the progression of diabetic nephropathy and neuropathy and act as antioxidants. Ongoing studies have elucidated protective roles for them in both memory-related disorders and cancer. INTRODUCTIONIn recent years, stressful and fiercely competitive lifestyles and food habits have compounded the problems of hypertension. Long-standing and stressful, progressively rising hypertension can lead to many disorders, including myocardial infarction (MI), cerebrovascular events, congestive heart failure, peripheral arterial insufficiency, premature mortality 1 and renal dysfunction leading to glomerulosclerosis and kidney artery aneurysm. 2 A number of therapies are available, but angiotensin-converting enzyme (ACE) inhibitors have been the preferred first-line therapy for hypertension, congestive heart failure, left ventricular (LV) systolic dysfunction and MI. 3,4 ACE inhibitors (ACEis) have been in use for the past two decades, and the interest in them is still growing. Recently, the discovery of domain-selective ACEis and new members of the renin-angiotensin system (RAS) (that is, angiotensin-converting enzyme 2) have again fueled the interest of researchers. Some new studies have expanded the already impressive clinical profile of ACEis. This review traces some already known and new facets of ACE inhibition and introduces new advances in the designing of a new generation of ACEis.

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Effect of angiotensin-converting-enzyme (ACE) inhibitor trandolapril on human diabetic neuropathy: randomised double-blind controlled trial

Cited by 267 publications

References 26 publications

Why Not to Use the Handgrip Test in the Assessment of Cardiovascular Autonomic Neuropathy Among Patients with Diabetes Mellitus?

Why Not to Use the Handgrip Test in the Assessment of Cardiovascular Autonomic Neuropathy Among Patients with Diabetes Mellitus?

Cardiovascular Autonomic Neuropathy

Reinventing the ACE inhibitors: some old and new implications of ACE inhibition

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