Microvascular Angina: Diagnosis and Management.
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ABSTRACT:
SUBMITTER: Aldiwani H
PROVIDER: S-EPMC8674627 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Microvascular angina (MVA), historically called cardiac syndrome X, refers to angina with nonobstructive coronary artery disease. This female-predominant cardiovascular disorder adds considerable health-related costs due to repeated diagnostic angiography and frequent hospital admissions. Despite the high prevalence of this diagnosis in patients undergoing coronary angiography, it is still a therapeutic challenge for cardiologists. Unlike obstructive coronary artery disease, with multiple evidence-based therapies and management guidelines, little is known regarding the management of MVA. During the last decade, many therapeutic interventions have been suggested for the treatment of MVA. However, there is a lack of summarization tab and update of current knowledge about pharmacologic management of MVA, mostly due to unclear pathophysiology. In this article, we have reviewed the underlying mechanisms of MVA and the outcomes of various medications in patients with this disease. Contrary to vasospastic angina in which normal angiogram is observed as well, nitrates are not effective in the treatment of MVA. Beta-blockers and calcium channel blockers have the strongest evidence of improving the symptoms. Moreover, the use of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, statins, estrogen, and novel antianginal drugs has had promising outcomes. Investigations are still ongoing for vitamin D, omega-3, incretins, and n-acetyl cysteine, which have resulted in beneficial initial outcomes. We believe that the employment of the available results and results of the future large-scale trials into cardiac care guidelines would help reduce the global cost of cardiac care tremendously.
| S-EPMC9626221 | biostudies-literature
Project description:BackgroundIn patients with angina and nonobstructive coronary artery disease (NOCAD), confirming symptoms due to coronary microvascular dysfunction (CMD) remains challenging. Cardiac magnetic resonance (CMR) assesses myocardial perfusion with high spatial resolution and is widely used for diagnosing obstructive coronary artery disease (CAD).ObjectivesThe goal of this study was to validate CMR for diagnosing microvascular angina in patients with NOCAD, compared with patients with obstructive CAD and correlated to the index of microcirculatory resistance (IMR) during invasive coronary angiography.MethodsFifty patients with angina (65 ± 9 years of age) and 20 age-matched healthy control subjects underwent adenosine stress CMR (1.5- and 3-T) to assess left ventricular function, inducible ischemia (myocardial perfusion reserve index [MPRI]; myocardial blood flow [MBF]), and infarction (late gadolinium enhancement). During subsequent angiography within 7 days, 28 patients had obstructive CAD (fractional flow reserve [FFR] ≤0.8) and 22 patients had NOCAD (FFR >0.8) who underwent 3-vessel IMR measurements.ResultsIn patients with NOCAD, myocardium with IMR <25 U had normal MPRI (1.9 ± 0.4 vs. controls 2.0 ± 0.3; p = 0.49); myocardium with IMR ≥25 U had significantly impaired MPRI, similar to ischemic myocardium downstream of obstructive CAD (1.2 ± 0.3 vs. 1.2 ± 0.4; p = 0.61). An MPRI of 1.4 accurately detected impaired perfusion related to CMD (IMR ≥25 U; FFR >0.8) (area under the curve: 0.90; specificity: 95%; sensitivity: 89%; p < 0.001). Impaired MPRI in patients with NOCAD was driven by impaired augmentation of MBF during stress, with normal resting MBF. Myocardium with FFR >0.8 and normal IMR (<25 U) still had blunted stress MBF, suggesting mild CMD, which was distinguishable from control subjects by using a stress MBF threshold of 2.3 ml/min/g with 100% positive predictive value.ConclusionsIn angina patients with NOCAD, CMR can objectively and noninvasively assess microvascular angina. A CMR-based combined diagnostic pathway for both epicardial and microvascular CAD deserves further clinical validation.
| S-EPMC5835222 | biostudies-literature
Project description: Not available
| S-EPMC7035719 | biostudies-literature
Project description:In women receiving evaluation for suspected ischemic symptoms, a "normal" diagnosis is five times more common than it is in men. These women are often labeled as having cardiac syndrome X, also known as microvascular angina (MVA). MVA is defined as angina pectoris caused by abnormalities of the small coronary arteries, and is characterized by effort chest pain and evidence of myocardial ischemia with a non-invasive stress test, although the coronary arteries can appear normal or near normal by angiography. MVA patients are often neglected due to the assumption of a good prognosis. However, MVA has important prognostic implications and a proper diagnosis is necessary in order to relieve the patients' symptoms and improve clinical outcomes. The coronary microvasculature cannot be directly imaged using coronary angiography, due to the small diameter of the vessels; therefore, the coronary microvascular must be assessed functionally. Treatment of MVA initially includes standard anti-ischemic drugs (β-blockers, calcium antagonists, and nitrates), although control of symptoms is often insufficient. In this review, we discuss the pathophysiology, diagnosis, and treatment of MVA.
| S-EPMC4351318 | biostudies-literature
Project description:AimsCoronary microvascular dysfunction and/or vasospasm are potential causes of ischaemia in patients with no obstructive coronary artery disease (INOCA). We tested the hypothesis that these patients also have functional abnormalities in peripheral small arteries.Methods and resultsPatients were prospectively enrolled and categorised as having microvascular angina (MVA), vasospastic angina (VSA) or normal control based on invasive coronary artery function tests incorporating probes of endothelial and endothelial-independent function (acetylcholine and adenosine). Gluteal biopsies of subcutaneous fat were performed in 81 subjects (62 years, 69% female, 59 MVA, 11 VSA, and 11 controls). Resistance arteries were dissected enabling study using wire myography. Maximum relaxation to ACh (endothelial function) was reduced in MVA vs. controls [median 77.6 vs. 98.7%; 95% confidence interval (CI) of difference 2.3-38%; P = 0.0047]. Endothelium-independent relaxation [sodium nitroprusside (SNP)] was similar between all groups. The maximum contractile response to endothelin-1 (ET-1) was greater in MVA (median 121%) vs. controls (100%; 95% CI of median difference 4.7-45%, P = 0.015). Response to the thromboxane agonist, U46619, was also greater in MVA (143%) vs. controls (109%; 95% CI of difference 13-57%, P = 0.003). Patients with VSA had similar abnormal patterns of peripheral vascular reactivity including reduced maximum relaxation to ACh (median 79.0% vs. 98.7%; P = 0.03) and increased response to constrictor agonists including ET-1 (median 125% vs. 100%; P = 0.02). In all groups, resistance arteries were ≈50-fold more sensitive to the constrictor effects of ET-1 compared with U46619.ConclusionsSystemic microvascular abnormalities are common in patients with MVA and VSA. These mechanisms may involve ET-1 and were characterized by endothelial dysfunction and enhanced vasoconstriction.Clinical trial registrationClinicalTrials.gov registration is NCT03193294.
| S-EPMC6284165 | biostudies-literature
Project description:Refractory angina (RA) is defined as debilitating anginal symptoms despite the optimal guideline-directed combination of medical, percutaneous, and surgical therapies. Often referred to as "no option", these patients represent a significant unmet clinical need for healthcare institutions. Due to the ageing of the population, and increased survival from coronary artery disease, the number of patients with RA is expected to rise exponentially. Despite the developments of novel technologies for the treatment of RA, none of them found wide clinical application (to date). Microvascular dysfunction, alone or in combination with epicardial coronary disease, is thought to contribute significantly to refractory angina. However, most of the techniques developed to improve RA symptoms have not been tested specifically on patients with microvascular dysfunction. This review discusses the recent developments in the treatment of RA, and gives some perspectives on the future of these techniques.
| S-EPMC7460172 | biostudies-literature
Project description:Nearly 40% of patients presenting to the catheter laboratory with angina have non-obstructed coronary arteries (ANOCA), an umbrella term that encompasses distinct pathophysiological entities, such as coronary artery spasm. Coronary artery spasm leads to sudden reversible coronary flow attenuation, which clinically manifests as vasospastic angina (VSA). VSA is associated with poor quality of life and an increased risk of major adverse cardiac events. However, the pathophysiological mechanisms underlying this phenomenon are incompletely understood, which has resulted in limited therapeutic options for patients afflicted with this condition. The past decade has seen a surge in new research being conducted in the field of ANOCA and VSA. This review article provides a comprehensive summary of the underlying pathophysiological mechanisms of VSA and the current therapeutic options. We also appraise the current diagnostic approach in patients with suspected VSA.
| S-EPMC9872780 | biostudies-literature
Project description:ImportanceThe role of the coronary venous circulation in regulating myocardial perfusion and its potential in treating microvascular angina is unexplored.ObjectiveTo evaluate whether an increase in coronary venous pressure modifies microvascular resistance in patients with microvascular angina.Design, setting, and participantsThis was a blinded, sham-controlled, crossover, randomized clinical trial that enrolled participants between November 2021 and January 2023. Participants for this physiology end point study were recruited from the Cardiology Center of the University of Medicine in Mainz, Germany. Patients with moderate/severe angina pectoris (Canadian Cardiovascular Society class 2-4) due to microvascular dysfunction (as defined by the thermodilution-based index of microvascular resistance >25 mm Hg × s). Exclusion criteria were epicardial coronary disease, second- and third-degree atrioventricular block, severe valvular heart disease, cardiomyopathy, and pulmonary or kidney disease.InterventionInflation of an undersized balloon placed in the cardiac coronary sinus (CS), hereafter referred to as balloon and the deflated balloon in the right atrium, referred to as sham. Measurements were performed at rest and during maximal coronary hyperemia. Both patients and final assessors were blinded to the randomization sequence.Main outcomes and measuresHemodynamic parameters, including aortic (Pa) and distal (Pd) coronary pressure, coronary sinus pressure (Pcs), right atrial pressure (Pra), and the mean transit time (inverse of blood flow [Tmn]), were measured.ResultsA total of 20 patients (median [IQR] age, 69 [64-75] years; 11 female [55.0%]) were included in the study. Two patients (10%) had diabetes, 6 (30%) had hypercholesterolemia, 15 (75%) had hypertension, and 3 (15%) were active smokers. The inflation of the CS balloon caused a significant increase in CS pressure at rest and during hyperemia (300% and 317% increase, respectively, compared with sham, both P < .001), a decrease in hyperemic distal coronary pressure (median [IQR], sham: 92 [80-100] mm Hg; balloon: 79 [75-93] mm Hg; P = .01) and mean transit time (sham: 0.39 [0.23-0.62] s; balloon: 0.26 [0.17-0.46] s; P = .008). As a result, CS occlusion led to a decrease in both resting coronary resistance (median [IQR], sham: 59 [37-87] mm Hg × s; balloon: 42 [31-67] mm Hg × s; P = .005) and the primary end point hyperemic coronary resistance (mean [IQR], sham: 31 [23-53] mm Hg × s; balloon: 14 [8-26] mm Hg × s; P < .001).Conclusion and relevanceIncreased coronary venous pressure led to a reduction of microvascular resistances in patients with microvascular angina, a mechanism with potential implications for the therapy of this complex disease.Trial registrationClinicalTrials.gov Identifier: NCT05034224.
| S-EPMC10448373 | biostudies-literature
Project description:Refractory angina (RA) is defined as chest pain caused by coronary ischemia in patients on maximal medical therapy and is not amenable to revascularization despite advanced coronary artery disease (CAD). The long-term prognosis has improved with optimal medical therapy including risk factor modification. Still, patients are left with major impairment in quality of life and have high resource utilization with limited treatment options. We review the novel invasive and noninvasive therapies under investigation for RA.
| S-EPMC9275781 | biostudies-literature
Project description:With improvements in survival from coronary artery disease (CAD) and an ageing population, refractory angina (RA) is becoming an increasingly common clinical problem facing clinicians in routine clinical practice. These patients experience chronic symptoms in the context of CAD, characterised by angina-type pain, which is uncontrolled despite optimal pharmacological, interventional and surgical therapy. Although mortality rates are no worse in this cohort, patients experience a significantly impaired quality of life with disproportionately high utilisation of healthcare services. It has been increasingly recognised that the needs of RA patients are multifactorial and best provided by specialist multi-disciplinary units. In this review, we consider the variety of therapies available to clinicians in the management of RA and discuss the promise of novel treatments.
| S-EPMC6159461 | biostudies-other