A “statin holiday” involves temporarily discontinuing your statin medication—typically for four to six weeks—to observe whether your symptoms improve. This break can provide valuable insights into whether statins are the culprit or if other factors, such as unrelated medical conditions or lifestyle changes, are contributing to your symptoms. The blog and podcast explain how a simple visual diary can be used to help assess the impact of the N-of-1 trial.

However, it’s essential to discuss this approach with your healthcare provider before making any changes. Stopping statins abruptly without a plan may increase your cardiovascular risk, especially if you have a history of heart disease or other high-risk factors.

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Aspirin, or acetylsalicylic acid, is one of the oldest and most widely used medications in the world.

Well known for its analgesic effects, it was later discovered to be effective (in much smaller doses) in preventing platelet aggregation that had a pivotal role in arterial thrombosis.

Its  role in inhibiting platelet activity has made it a cornerstone in the prevention and treatment of arterial thrombosis. In this article, we will explore the fascinating role of platelets in acute coronary thrombosis, the mechanisms by which aspirin exerts its protective effects, and the clinical considerations for its use.

https://www.scvc.co.uk/naked-heart/aspirin/

The timing of intervention in aortic stenosis is critical. Delaying surgery or transcatheter procedures until symptoms become severe or complications arise can lead to poorer outcomes. Conversely, intervening too early may expose patients to unnecessary procedural risks. For exceptionally fit individuals aged 75-85, timely intervention can be particularly advantageous, as they may tolerate surgical aortic valve replacement (SAVR) better than expected for their age. In these cases, earlier treatment may prevent irreversible damage to the heart and reduce the risks associated with waiting until the disease progresses further.

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The aortic valve is the ‘non return’ valve positioned to prevent oxygenated blood leaving the heart from refluxing back into the heart after each heart contraction. When this valve narrows, it restricts the flow of blood leaving the heart in a condition known as ‘aortic stenosis’.

Aortic stenosis (AS) is a progressive and potentially life-threatening condition. It predominantly affects older adults and has significant implications for cardiovascular health, life expectancy, and quality of life.  The incidence of AS is climbing because of increased life expectancy. Timely intervention, especially in symptomatic patients or those with progressing stenosis, is essential to optimise outcomes. This article explores the nuances of AS diagnosis, treatment decisions, and the importance of patient involvement in the care pathway.

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Angina pectoris, commonly known simply as angina, is not a diagnosis but a clinical syndrome characterised by chest pain or discomfort resulting from myocardial ischaemia—conditions under which the blood flow to the heart muscle is insufficient to meet its metabolic demands.

This symptom can be the first indicator of coronary artery disease (CAD), the most common type of heart disease, which is why recent onset angina is usually investigated as a priority. Many people are not aware that there are many other causes of angina such as aortic valve narrowing (aortic stenosis), anaemia (low red cell count),  coronary spasm and even a mysterious cause that mimics the atherosclerotic cause called 'syndrome X' or microvascular angina. 

In this longer podcast angina is discussed in greater depth.

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A young and healthy heart can double its stroke volume in a heartbeat. However, this capability diminishes with an ageing heart, especially one that has been subjected to high blood pressure, heart valve issues or metabolic conditions such as poor glucose control over many years. These factors cause the left ventricle to stiffen in many people as they age, limiting their left ventricle's  ability to change its stroke volume. Consequently, any change in cardiac output in older individuals, or those with a stiff heart, increasingly relies on increasing the heart rate.

If the heart rate fails to increase with physical activity, cardiac output becomes constrained. Somewhat scarily, doctors call this "Chronotropic Incompetence" or "CI" for short. 

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Getting your head around the difference between heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF) is a challenge for everyone. This is a technical discussion about why a stiff heart causes poor left ventricular suction and diastolic dysfunction.

In part 2 of the podcast their is a major focus on what lifestyle measures during mid life may help fend off the risk of heart failure in later life. 

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Beta blockers work on the beta receptor situated on the surface of cells that are affected by circulating adrenaline which the body releases in times of stress. Small amounts of adrenaline circulate, even at rest and help determine the resting heart rate and cardiac output. They also have a direct action on the Sinoatrial node which sets the heart rate and the AV node, which becomes very important in patients prone to atrial fibrillation and flutter. Beta blockers have been developed over 50 years and are used to treat a wide range of conditions, including palpitations due to arrhythmia, high blood pressure, anxiety, migraine to name just a few. For a cardiologist, beta blockers are a commonly used medication, possibly because we live in a high stress world and patients come to us with symptoms that are often improved by taking blockers. Cardioselective beta blockers are more popular as they are far less likely to trigger bronchoconstriction or asthma. Here are a few points that are often raised by our patients.

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Bradycardia, or a slow heart rate, is a term you might have come across in a medical report or perhaps during a routine checkup. For many, hearing that their heart rate is "too low" can trigger concern. But what does bradycardia actually mean? And when does a slow pulse become something to address with a healthcare professional? Let’s dive deeper into the causes, symptoms, and treatment options, to help demystify bradycardia and highlight when it is a natural variation and when it requires medical attention.

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In atrial fibrillation, the atrial tissue quivers at approximately 600 cycles per minute, which means that it has no useful pumping function. The left atrium in patients with atrial fibrillation, merely acts as a passive conduit between the lungs and the left ventricle. It no longer serves to prime the left ventricle, and as a result, there may be less blood entering the heart during diastole and thus less 'priming' occurs, so cardiac output may fall. If ever you have experienced a car's turbo charger going 'on the blink' you will know that the car still GOES, but not very well, since it too suffers loss of output.  The left atrial pressure in many such cases will increase, causing oedema or fluid in the alveolar space, reducing gas exchange and contributing to the symptom of breathlessness.

Any stiffening of the left ventricle that for example accompanies old age, poor glycaemic control or indeed any condition that causes thickening of the left ventricle, such as hypertension or cardiomyopathy, therefore has a big impact on the ability of the left ventricle to relax and suck blood through from the left atrium and joining pulmonary veins, creating  backup of blood into the lung tissue.

For more on this topic and other related blog articles and podcasts see

https://www.scvc.co.uk/naked-heart/why-do-patients-in-atrial-fibrillation-get-breathless/