Online Clinical Case Study (April 2013)

The content of the Office Cardiology Series is provided by:
Dr. LAM Chiu Wah FHKCP, FHKAM (Med), FRCP (Edin), Specialist in Cardiology
Dr. LI Siu Lung, Steven FHKAM (Med), FRCP (Glasg), FRCP (Edin), FRCP (Lond), Specialist in Cardiology
Dr. WONG Shou Pang, Alexander FRCP, FHKAM (Med), FHKCP, Specialist in Cardiology


New guidelines for the diagnosis and management of patients with stable ischaemic heart disease


The following medications prevent myocardial infarction and death in patients with stable ischemic heart disease:
a. Dipyridamole
b. Oestrogen therapy in postmenopausal women
c. Vitamin C, vitamin E and beta-carotene supplementation
d. Treatment of elevated homocysteine with folate or vitamins B6 and B12
e. None of the above


For patients on beta blocker or calcium channel blocker monotherapy whose symptoms are not controlled and the other option (calcium channel blocker or beta blocker) is contraindicated or not tolerated, the following drug(s) may be helpful.
a. Long-acting nitrates
b. Ranolazine
c. Nicorandil
d. Ivabradine
e. All of the above


1. e 2. e

Dipyridamole has antiplatelet effects but does not have a proven role in patients with stable ischaemic heart disease. In the Persantine-Aspirin Reinfarction Study, the combination of aspirin and dipyridamole was not clearly superior to aspirin alone in preventing reinfarction. Moreover, dipyridamole vasodilates coronary resistance vessels and can provoke exercise-induced myocardial ischaemia.

Beneficial effects of exogenous oestrogen include an increase in HDL cholesterol, a decrease in LDL cholesterol, and enhanced endothelial function. However, clinical trials in women have failed to confirm a decrease in cardiovascular events with hormone therapy. In Heart and Estrogen/Progesterone Replacement Study, 2,763 postmenopausal women with coronary artery disease were follow-up for 4.4 years. Despite an 11% lower level of LDL cholesterol and a 10% higher level of HDL cholesterol in the hormone therapy group, continuous oestrogen-progestin therapy did not reduce cardiovascular events.

Studies of the mechanisms of atherosclerosis suggest that antioxidants might be protective. Additionally, cardiovascular protection has been associated with dietary patterns high in antioxidants, i.e. from fruits and vegetables. Large clinical trials have studied the effect of supplementation with antioxidant vitamins, such as vitamin E, vitamin C, and beta-carotene, on secondary prevention of CHD. There is no convincing evidence of benefit alone or in combination. The Heart Protection Study randomized 20,536 patients who had a history of cardiovascular disease, or diabetes mellitus to five years of antioxidant vitamin supplementation (vitamin E, vitamin C, and beta-carotene) or placebo. Supplementation had no effect on cardiovascular mortality and nonfatal myocardial infarction.

Homocysteine has primary atherogenic and prothrombotic properties. Observational studies have demonstrated that the serum homocysteine level is a strong, independent risk factor for ischemic events. Homocysteine levels can be lowered by folic acid or B-vitamins. Trials of folate and vitamin B supplementation, however, consistently failed to demonstrate a decrease in cardiovascular morbidity or mortality rates. In HOPE 2 (Heart Outcome in Prevention) trial, 5,522 patients with known vascular disease or diabetes were randomly assigned to receive supplementation with folic acid, vitamin B6, and vitamin B12. No benefit was found after five years.

The 2011 NICE guidelines of stable angina suggests a long-acting nitrate, ivabradine, nicorandil or ranolazine may be considered for patients on beta blocker or calcium channel blocker monotherapy whose symptoms are not controlled and the other option (calcium channel blocker or beta blocker) is contraindicated or not tolerated.

Nitrates are effective in the treatment of all forms of angina. While they act as vesodilators, coronary vasodilators, and modest arteriolar dilators, the primary antiischemic effect of nitrates is to decrease myocardial oxygen demand by producing systemic vasodilation more than coronary vasodilation. This systemic vasodilation reduces left ventricular systolic wall stress.

The mechanism of action of ranolazine has not been fully elucidated, but it is believed to act by selective inhibition of late sodium influx across the sarcolemma, which attenuates the abnormalities of ventricular repolarization and contractility associated with myocardial ischaemia. In the CARISA trial, ranolazine reduces the frequency of angina, improves exercise performance, and delays the development of exerciseinduced angina and ST-segment depression in patients receiving background antianginal therapy of calcium channel blocker or atenolol.

Nicorandil is a nitrate derivative of nicotinamide. Nicorandil is believed to have a dual mechanism of action. Specifically, nicorandil provides a nitrate moiety that dilates epicardial coronary arteries and systemic venous capacitance vessels. In addition, nicorandil opens ATP-sensitive potassium channels (KATP) in vascular smooth muscle cells, thereby dilating arterial resistance vessels in the peripheral and coronary circulations.

Ivabradine is a specific inhibitor of the If current of pacemaker cells in the sinoatrial node at concentrations that do not inhibit other cardiac currents. This action results in heart rate reduction, prolonging diastole and thereby improving myocardial oxygen balance. Ivabradine has no effect on blood pressure, myocardial contractility, or intracardiac conduction parameters. Ivabradine improves exercise capacity and reduces anginal frequency in comparison to atenolol among patients with chronic stable angina.

1. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Guideline for the Diagnosis and Management of Patients With Stable Ischemic Heart Disease. Circulation. 2012; 126: e354-471.
2. Management of stable angina. National Clinical Guideline Centre. Management of stable angina. London (UK): National Institute for Health and Clinical Excellence (NICE); July 2011.


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Dermatology Series 皮膚科病例研究

A gentleman with itchy rash over buttock

A 56-year-old gentleman with history of diabetes complained of itchy rash over buttock for few weeks which was worsening in nature. Physical examination showed well defined scaly patches over the buttock. There was no other similar lesion over the other part of the body.

The content of the Dermatology Series is provided by:
Dr. CHAN Hau Ngai, Kingsley, Dr. TANG Yuk Ming, William, Dr. KWAN Chi Keung, and Dr. LEUNG Wai Yiu
Specialists in Dermatology & Venereology



What is the clinical diagnosis?

The patient is suffering from tinea cruris.

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What are the differential diagnoses?

The differential diagnoses include: candidiasis, dermatitis, psoriasis, erythrasma, Hailey-Hailey disease and intertrigo.

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Who are more prone to this skin condition?

Obese people and diabetic patients are more prone to having tinea cruris. People who always wear tight fitting clothes for a long period of time may develop this skin disease.

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How is this skin condition diagnosed?

Tinea cruris can usually be diagnosed clinically. For more complicated cases, skin scrapping over the skin lesion for fungal microscopy (potassium hydroxide [KOH] wet mount) and culture, or even using skin biopsy (using periodic acid- Schiff stain [fungal elements appear pink] or methenamine silver stains (fungal elements appear brown or black) may be needed to confirm the diagnosis.

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5. What are the treatments?
  Most patients are treated with topical antifungal agents of the imidazole or allylamine family. For those cases with extensive or recalcitrant infection, oral antifungal medications, including terbinafine and itraconazole, may be needed.
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