The J-Curve in Arterial Hypertension: Fact or Fallacy?

Tsika, Evangelia P.; Poulimenos, Leonidas; Boudoulas, Konstantinos Dean; Manolis, Athanasios

doi:10.1159/000362381

Cited by 25 publications

(18 citation statements)

References 50 publications

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“…Even in the presence of diabetes and other risk factors, no reason exists to adopt an aggressive blood-pressure-lowering treatment, as previously suggested. A meta-analysis showed that in patients with diabetes and a baseline systolic blood pressure level <140 mmHg, further blood-pressure lowering resulted in an increased risk of cardiovascular death 73 (FIG. 4).…”

Section: Guideline Recommendationsmentioning

confidence: 99%

“…No validated threshold exists for high versus low blood pressure in patients with coronary artery disease. Considering the available data, a threshold of 130 mmHg systolic and 80 mmHg diastolic is reasonable 72,73 . In patients with lower blood pressure, the use of ivabradine (if associated with a concomitant increase in heart rate), ranolazine, or trimetazidine is preferable (FIG.…”

Section: Guideline Recommendationsmentioning

confidence: 99%

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A 'diamond' approach to personalized treatment of angina

et al. 2017

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Chronic stable angina pectoris is the most prevalent symptomatic manifestation of ischaemic heart disease, and its management is a priority (BOX 1). Current clinical guidelines recommend antianginal therapy to control symptoms, before considering coronary artery revasculariza tion [1][2][3][4] . However, revascularization by either percutaneous coronary angioplasty or CABG surgery is indicated in patients who have significant artery steno sis (50% left main narrowing or proximal three-vessel disease) to reduce myocardial ischaemia and its adverse clinical manifestation. Antianginal agents are approved by documenting that they improve total exercise duration, together with a reduction in daily frequency of chronic stable angina compared with placebo and/or equivalence to an active comparator. Cardiovascular outcomes, although highly advocated, are not a pre requisite for regulatory approval. None of the antianginal drugs has been proved to reduce cardiovascular mortality or the rate of myocardial infarction. When patients are optimally treated, mortality for chronic stable angina is low, which might explain why all trials designed to improve prognosis have been negative. Guidelines recom mend a first-choice and a second-choice approach, based more on tradition and expert opinion, rather than evidence. This categorical approach has been questioned in the past couple of years 5-8 . Newer antianginal drugs, which are classified as second choice, have more evidence-based clinical data that are more contemporary to support their use than is available for the traditional first-choice drugs. Equally, the often-needed combin ation of double or triple therapy is based on expert opinion and not related to the underlying pathophysio logy. What constitutes optimal antianginal treatment, therefore, varies considerably between countries, and the majority of doctors treat their patients according to their own preconceptions.A group of experts with experience and interest in chronic stable angina met at the University of Ferrara, Italy, to discuss an individualized approach to medical treatment of chronic stable angina, on the basis E X P E RT C O N S E N S U S D O C U M E N TA 'diamond' approach to personalized treatment of angina Abstract | In clinical guidelines, drugs for symptomatic angina are classified as being first choice (β-blockers, calcium-channel blockers, short-acting nitrates) or second choice (ivabradine, nicorandil, ranolazine, trimetazidine), with the recommendation to reserve second-choice medications for patients who have contraindications to first-choice agents, do not tolerate them, or remain symptomatic. No direct comparisons between first-choice and second-choice treatments have demonstrated the superiority of one group of drugs over the other. Meta-analyses show that all antianginal drugs have similar efficacy in reducing symptoms, but provide no evidence for improvement in survival. The newer, second-choice drugs have more evidence-based clinical data that are more contemporary than is available for tr...

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Section: Guideline Recommendationsmentioning

confidence: 99%

Section: Guideline Recommendationsmentioning

confidence: 99%

A 'diamond' approach to personalized treatment of angina

et al. 2017

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“…A faster heart rate during therapy for hypertension may be associated with adverse events, regardless of the extent of changes in blood pressure. Thus, the so-called J-curve phenomenon in arterial hypertension may at least partially be related to an increase in heart rate and not only to changes in blood pressure [54]. …”

Section: Heart Rate and Survival After Therapeutic Interventionsmentioning

confidence: 99%

Heart Rate, Life Expectancy and the Cardiovascular System: Therapeutic Considerations

Boudoulas¹,

Borer²,

Boudoulas³

2015

Cardiology

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It has long been known that life span is inversely related to resting heart rate in most organisms. This association between heart rate and survival has been attributed to the metabolic rate, which is greater in smaller animals and is directly associated with heart rate. Studies have shown that heart rate is related to survival in apparently healthy individuals and in patients with different underlying cardiovascular diseases. A decrease in heart rate due to therapeutic interventions may result in an increase in survival. However, there are many factors regulating heart rate, and it is quite plausible that these may independently affect life expectancy. Nonetheless, a fast heart rate itself affects the cardiovascular system in multiple ways (it increases ventricular work, myocardial oxygen consumption, endothelial stress, aortic/arterial stiffness, decreases myocardial oxygen supply, other) which, in turn, may affect survival. In this brief review, the effects of heart rate on the heart, arterial system and survival will be discussed.

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“…Although there is not a validated threshold dividing SCHD patients into a high and low BP levels, a threshold of 120 mmHg in systolic blood pressure can be used as a reference [83,84]. Some have recently advocated a threshold of 100 mmHg of systolic blood pressure, below which not to further push treatment with antianginal drugs that have vasodilating properties [85] ).…”

Section: Blood Pressurementioning

confidence: 99%