Haemodynamic and Metabolic Effects of Timolol (Blocadren®) on Ischaemic Myocardium

Simonsen, Svein; Ihlen, Halfdan; Kjekshus, John

doi:10.1111/j.0954-6820.1983.tb03757.x

Cited by 31 publications

(6 citation statements)

References 21 publications

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“…Similarly, in patients with angina pectoris, beta-blockade does not reduce myocardial oxygen demand or ischemia if angina is induced by atrial pacing (41).…”

Section: Myocardial Ischemiamentioning

confidence: 99%

Resting Heart Rate in Cardiovascular Disease

Fox

Borer

Camm

et al. 2007

Journal of the American College of Cardiology

921

627

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The importance of resting heart rate (HR) as a prognostic factor and potential therapeutic target is not yet generally accepted. Recent large epidemiologic studies have confirmed earlier studies that showed resting HR to be an independent predictor of cardiovascular and all-cause mortality in men and women with and without diagnosed cardiovascular disease. Clinical trial data suggest that HR reduction itself is an important mechanism of benefit of beta-blockers and other heart-rate lowering drugs used after acute myocardial infarction, in chronic heart failure, and in stable angina pectoris. Pathophysiological studies indicate that a relatively high HR has direct detrimental effects on the progression of coronary atherosclerosis, on the occurrence of myocardial ischemia and ventricular arrhythmias, and on left ventricular function. Studies have found a continuous increase in risk with HR above 60 beats/min. Although it may be difficult to define an optimal HR for a given individual, it seems desirable to maintain resting HR substantially below the traditionally defined tachycardia threshold of 90 or 100 beats/min. These findings suggest that the potential role of HR and its modulation should be considered in future cardiovascular guidance documents.

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“…Similarly, in patients with angina pectoris, beta-blockade does not reduce myocardial oxygen demand or ischemia if angina is induced by atrial pacing (41).…”

Section: Myocardial Ischemiamentioning

confidence: 99%

Resting Heart Rate in Cardiovascular Disease

Fox

Borer

Camm

et al. 2007

Journal of the American College of Cardiology

921

627

View full text Add to dashboard Cite

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“…By reducing peripheral lipolysis, this pharmacological class lowers the levels of FFA in the blood and allows a change in the heart's energy metabolism that increases the use of carbohydrates [36]. Through these metabolic processes, betablockers are responsible for this substrate competition's decreased myocardial FFA uptake and increased glucose utilization [37,38]. A decrease in FFA delivery and an increase in the availability of arterial glutamate, which is highly advantageous for myocardial tissue as it can serve as both aerobic and anaerobic fuel, making it a particularly versatile substrate [38], are both likely to be responsible for the increase in carbohydrate metabolism in the heart that was observed after a beta-blockade [39,40].…”

Section: Betablockersmentioning

confidence: 99%

Metabolic Approaches for the Treatment of Dilated Cardiomyopathy

Spoladore

Pinto

Daus

et al. 2023

JCDD

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In dilated cardiomyopathy (DCM), where the heart muscle becomes stretched and thin, heart failure (HF) occurs, and the cardiomyocytes suffer from an energetic inefficiency caused by an abnormal cardiac metabolism. Although underappreciated as a potential therapeutic target, the optimal metabolic milieu of a failing heart is still largely unknown and subject to debate. Because glucose naturally has a lower P/O ratio (the ATP yield per oxygen atom), the previous studies using this strategy to increase glucose oxidation have produced some intriguing findings. In reality, the vast majority of small-scale pilot trials using trimetazidine, ranolazine, perhexiline, and etomoxir have demonstrated enhanced left ventricular (LV) function and, in some circumstances, myocardial energetics in chronic ischemic and non-ischemic HF with a reduced ejection fraction (EF). However, for unidentified reasons, none of these drugs has ever been tested in a clinical trial of sufficient size. Other pilot studies came to the conclusion that because the heart in severe dilated cardiomyopathy appears to be metabolically flexible and not limited by oxygen, the current rationale for increasing glucose oxidation as a therapeutic target is contradicted and increasing fatty acid oxidation is supported. As a result, treating metabolic dysfunction in HF may benefit from raising ketone body levels. Interestingly, treatment with sodium-glucose cotransporter-2 inhibitors (SGLT2i) improves cardiac function and outcomes in HF patients with or without type 2 diabetes mellitus (T2DM) through a variety of pleiotropic effects, such as elevated ketone body levels. The improvement in overall cardiac function seen in patients receiving SGLT2i could be explained by this increase, which appears to be a reflection of an adaptive process that optimizes cardiac energy metabolism. This review aims to identify the best metabolic therapeutic approach for DCM patients, to examine the drugs that directly affect cardiac metabolism, and to outline all the potential ancillary metabolic effects of the guideline-directed medical therapy. In addition, a special focus is placed on SGLT2i, which were first studied and prescribed to diabetic patients before being successfully incorporated into the pharmacological arsenal for HF patients.

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“…Data from previous studies have shown that in 26 patients with angina pectoris, timolol (2.5 mg i.v) did not reduce myocardial oxygen demand or ischemia if angina is induced by atrial pacing [58]. In addition, Heidland et al [59] retrospectively analyzed 106 patients who underwent 2 coronary angiography procedures within 6 months, and demonstrated that the use of b-blockers was negatively correlated with plaque disruption [59].…”

Section: B-blockersmentioning

confidence: 99%

Heart Rate as a Therapeutic Target in Angina Pectoris

Androulakis¹,

Tousoulis²,

Papageorgiou³

et al. 2013

Current Pharmaceutical Design

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Heart rate is a major determinant of cardiac output and myocardial oxygen utilization and is increasingly being nominated as a modifiable risk factor for cardiovascular disease. Despite this evidence, screening strategies for preventing cardiovascular diseases do not include routine assessment of resting heart rate. Reasonably, heart rate reduction has been suggested as a useful approach against angina pectoris in subjects with acute or chronic coronary syndromes. Accordingly, reduction of heart rate in patients with stable angina could be an additional goal of therapy. Important data have shown retrospectively the beneficial effect of heart rate-lowering drugs, such as betaadrenoceptor antagonists, non-dihydropyridine calcium channel antagonists, as well as other agents, on several parameters in patients with coronary artery disease and stable angina. However, additional data are now being sought to assess the impact of this approach on clinical practice.

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Haemodynamic and Metabolic Effects of Timolol (Blocadren®) on Ischaemic Myocardium

Cited by 31 publications

References 21 publications

Resting Heart Rate in Cardiovascular Disease

Resting Heart Rate in Cardiovascular Disease

Metabolic Approaches for the Treatment of Dilated Cardiomyopathy

Heart Rate as a Therapeutic Target in Angina Pectoris

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