Occurrence Of Silent Myocardial Ischemia Research Articles

Caractéristiques des douleurs thoraciques au cours des syndromes coronariens aigus vus au service de cardiologie de Befelatanana (Madagascar)

IntroductionChest pain is one of the different elements of orientation for the diagnosis of acute coronary syndrome. Sometimes its clinical presentation is misleading. The objective of this study was to describe the characteristics of chest pain during an acute coronary syndrome in the cardiology department of the Joseph Raseta Befelatanana University Hospital Center, Antananarivo, Madagascar. MethodsWe carried out a cross-sectional, descriptive study of 10 months from January 2019 to October 2019. All patients diagnosed with acute coronary syndrome during this period were included. ResultsSixty-five cases were included. A “typical chest pain” was only encountered in 7.7% of cases. Advanced age (p = 0.04) and sedentary lifestyle (p = 0.03) were associated with the occurrence of silent myocardial ischemia, and. hypertension with a prolonged duration (≥15 minutes) of chest pain (p = 0.03). Dyslipidemia was associated with atypical irradiation of chest pain (p = 0.003). Alcoholism had an impact on pain triggered by effort (p = 0.01) and relieved by rest (p = 0.04). ConclusionThe current symptomatology of acute coronary syndrome is increasingly atypical. Knowledge of the factors that can influence the different characteristics of chest pain could serve as a benchmark in clinical practice in our population.

SILENT MYOCARDIAL ISCHEMIA AMONG ASYMPTOMATIC TYPE-2 DIABETIC PATIENTS

Objective: To determine the frequency of silent myocardial ischemia among asymptomatic type-2 diabetes mellitus patients. Methodology: This was a Cross sectional descriptive study conducted, after approval from the institutional ethical and research committee. A total of 90 asymptomatic type-2 diabetic patients were recruited for the present study. After informed written consent participants were subjected to a symptom-limited exercise tolerance test to detect the presence of silent myocardial ischemia. Descriptive statistics were applied to find frequencies and percentages for qualitative variables, and mean and standard deviation was used for quantitative variables. SPSS version22 was used for data analysis. Results: Among 90 type-2 asymptomatic diabetic patients, the frequency of silent myocardial ischemia was 36.7% (n=33). The frequency of silent myocardial ischemia among males and females was 57.6% and 42.4% respectively. Frequency of silent myocardial ischemia was found significantly more among patients with family history of CAD (60.6% vs 39.4%; p=0.029), prolonged duration of diabetes (15.2% vs 22.2% vs 63.6%; p=0.026) and group of patients with older age (9% vs 39.4 vs 51.6%; p=0.034). With respect to hypertension, smoking, obesity, and gender didn’t show statistically significant variation in the occurrence of silent myocardial ischemia. Conclusion: More than one third patients of asymptomatic type-2 diabetes mellitus had silent myocardial ischemia. Those with a family history of CAD, prolonged duration of diabetes, and participants with older age were more at risk of underlying silent myocardial ischemia.

Diabetic autonomic neuropathies as a major risk factor for silent myocardial ischemia and infarction: a literature review

A substantial number of myocardial infarctions (MIs) are asymptomatic or associated with mi-nor and atypical symptoms. These symptoms are often atypical or even absent, especially in di-abetic patients. A number of studies on this topic have shown that in the presence of myocardial ischemia and infarction, diabetic patients report angina less frequently than non-diabetic pa-tients. In this article review, we researched several published articles written about this subject and investigated the relationship between Diabetes Mellitus (DM) in patients and the occur-rence of silent myocardial ischemia and infarction due to the onset of diabetic neuropathy (DN), which is brought about by prolonged diabetes. Based on our research of published articles and studies, we found overwhelming evidence that supports the fact that diabetic autonomic neu-ropathy (DAN) is a major contributing factor in the morbidity of silent myocardial ischemia and infarction among patients suffering from DM. Â

Risk factors for silent myocardial ischemia in patients with well-controlled essential hypertension.

Silent myocardial ischemia (SMI) is frequently observed in patients with essential hypertension (EH). The major risk factor for SMI is uncontrolled blood pressure (BP), but SMI is also observed in patients with well-controlled BP. To evaluate the prevalence of SMI and the factors associated with SMI in EH patients with well-controlled BP. The medical records of 859 EH patients who underwent simultaneous 24-h ambulatory blood pressure monitoring (ABPM) and 24-h ambulatory electrocardiogram recording (AECG) were retrospectively evaluated. Each SMI episode was characterized by: (a) ST segment depression ≥0.5mm; (b) duration of ST segment depression >60s; and (c) reversibility of the ST segment depression. Overall 126 EH patients (14.7%) had at least one episode of SMI. The SMI events were more frequent among patients with poorly controlled compared to those with well-controlled BP [86/479 (17.95%) vs. 40/380 (10.52%), p<0.01]. Among EH patients with well-controlled BP, current and past smoking as well as the presence of an additional metabolic syndrome (MetS) constitutive element (obesity, impaired fasting glucose level or dyslipidemia) were significantly associated with the occurrence of SMI. In all EH patients with well-controlled BP and AECG evidence of SMI, there were one or more coronary artery stenotic lesions greater than 50% found at coronary angiography. In EH patients who are current smokers, or have one or more additional components of a MetS there is markedly reduced benefit associated with good BP control with regard to the occurrence of myocardial ischemia: in this patient category, an AECG may help detect this condition.

The relationship between lactate production in the myocardium and the development of chest pain in patients with coronary artery disease (CAD)

Silent myocardial ischemia (SMI) was recognized as early as the beginning of the 20th century. The consequences of silent ischemia can be grave because lack of symptoms and lack of symptom recognition. Early detection of SMI may prevent many episodes of sudden cardiac death annually. However, the role and behavior of the factors determining the occurrence of silent myocardial ischemia have not been fully established. To detect if there is a relationship between the level of lactate production in the myocardium and the development of chest pain in patients with coronary artery disease (CAD). This study was carried out in cardiology and biochemistry departments, Zagazig University on 46 patients (38 males) with coronary artery significant disease (>70% stenosis) including left anterior descending artery disease. Cannulation of coronary sinus with Amplatz left catheter was done and a pigtail catheter was introduced into the mid LV cavity. Right atrial pacing was done and the heart rate was increased stepwise 10 bpm/1 min until a maximum of 150 bpm or chest pain occurs or significant S–T segment depression occurs. LV gram for assessment of systolic function and blood samples were withdrawn from the LV and coronary sinus before and after pacing induced ischemia and the patients were classified into two groups according to development of chest pain (angina group; 28 patients) during pacing induced tachycardia or not (silent group; 18 patients). 24-h Holter ECG monitoring was done to all patients. Myocardial lactate production was significantly very high in angina group than in silent ischemia group; 10 patients (35.7%) had lactate diminished extraction and 18 patients (64.3%) had lactate production in response to pacing induced tachycardia in group 1 (angina group). All 18 patients (100%) in group 2 (silent ischemia group) had lactate diminished extraction in response to pacing induced tachycardia (<0.001). LV systolic function reduction in response to pacing induced ischemia was non significant between the 2 groups. Silent ischemic attacks represented >80% of total ischemic episodes during 24 h Holter ECG study and it occurred at lower heart rate than angina attacks ( P = 0.03). The magnitude of S–T segment depression was non significant between the two groups. In patients with coronary artery disease, myocardial lactate production is significantly higher in patients with angina than in patients with silent ischemia and as lactate is known (with other metabolic agents) to cause chest pain and this is considered an explanation (mechanism) for the occurrence of silent myocardial ischemia.

CLINICAL AND FUNCTIONAL CHARACTERISTICS OF PATIENTS AFTER Q-WAVE MYOCARDIAL INFARCTION DEPENDING ON THE METABOLIC SYNDROME PRESENCE OR ABSENCE

Aim. To study the clinical and functional parameters of patients after acute Q-wave myocardial infarction (Q-MI) depending on the concomitant metabolic syndrome (MS). Material and methods. Men after Q-MI (n=79; aged 51.7±8.9 years) were included into the study. Patients were divided into two groups depending on the MS presence or absence. Doppler echocardiography and determination of the serum C-reactive protein (CRP) level were performed in all patients on the 10-14 days after Q-MI, and treadmill test was performed in 25 patients. Results. Left ventricular ejection fraction was 12% lower and the CRP level was 2 times higher in MS patients versus these in non-MS patients (p<0.01). The silent segment ST depression ≥1.0 mm were more often observed in MS patients compared with this in non-MS patients (40% vs 5%; respectively, p<0.05). Conclusion. The MS presence complicates the post-infarction period by early heart failure progression, characterized by elevated CRP levels and more frequent occurrence of silent myocardial ischemia.

Silent myocardial ischemia is associated with altered plasma phospholipids

Timely and accurate confirmation of the occurrence of silent myocardial ischemia (SMI) is critical both for prevention and therapy management. Metabolomics assay may offer an alternative for SMI differentiation and altered biomolecule discovery in addition to traditional measures. In this study, plasma samples were obtained from 14 diagnosed SMI subjects and 25 healthy controls and analyzed by liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry in view of metabolomics. Obtained data were subjected to orthogonal signal correction partial least-squares discriminate analysis. Multi-variate statistic analysis indicated a clear separation between the two studied groups. Plasma concentration fluctuation of four kinds of phospholipids showed tight relationship with the occurrence of SMI, among which 1-linoleoylglycerophosphocholine (C18:2) was decreased statistically in SMI population (P=0.01). The plasma phospholipids' changes were before enzymatic alteration in SMI, which might be a useful complementary reference to facilitate SMI diagnosis.

Silent Myocardial Ischemia and High-Grade Ventricular Arrhythmias in Patients on Maintenance Hemodialysis

The occurrence of silent myocardial ischemia (SMI) and serious arrhythmias during hemodialysis (HD) has been well documented. However, it is unclear whether these changes are due to epicardial coronary artery disease (CAD). We conducted a prospective study to assess whether SMI and arrhythmias during HD correlated with angiographically demonstrable CAD. Twenty-three patients with end-stage renal disease on maintenance HD underwent 48-hour Holter monitoring, beginning 24 hours prior to a HD session. All patients underwent biochemical evaluation, coronary angiography, and echocardiography. Holter monitoring showed SMI during HD in 22% cases. A significant increase in the frequency of ventricular ectopics (VEs) was noted during and after HD. Patients who showed SMI during HD and VEs prior to initiation of dialysis were more likely to develop significant ventricular arrhythmias during and after HD. Epicardial CAD was documented in four patients, and it did not correlate with SMI. To conclude, HD is an arrhythmogenic process. SMI during dialysis is probably not due to epicardial CAD but predisposes to clinically significant ventricular arrhythmias during and after HD. The cause of SMI during HD in patients without demonstrable CAD needs further investigation.

Prevalence of episodes of ST-segment depression among mild-to-moderate hypertensive patients in northern Italy: the Cardioscreening Study.

To assess the prevalence of episodes of ST-segment depression in a population of consecutive patients with mild-to-moderate essential hypertension who are free of clinical signs of coronary artery disease. The study involved 28 Italian centers that enrolled 414 hypertensive patients (aged 50-70 years; diastolic blood pressure > or = 95-115 mmHg or systolic blood pressure > or = 150-220 mmHg, or both, 10 days after withdrawal of medications). Silent myocardial ischemia was assessed by means of exercise stress testing and 48 h Holter monitoring. An ischemic episode was defined as a horizontal or downward sloping ST-segment depression > or = 100 microV, occurring 80 ms after the J point, and lasting for at least 1 min. Of the 414 patients enrolled, 411 completed the exercise stress test. During the test significant ST-segment depression occurred for 25 patients (6.1%) and all episodes but one were asymptomatic and not associated with arrhythmias. Of the 396 patients for whom we analyzed a 48 h Holter recording, 43 (10.9%) had at least one episode of ST-segment depression and seven of these had also had one during the exercise stress test The median number of episodes per patient was five (range 1-19), median duration was 9 min (range 1-20 min), and the mean amplitude of the ST-segment depression was 190 +/- 180 microV. None of these episodes was associated with symptoms and all of them occurred under resting condition. Patients with (n = 61) and without (n = 335) ST-segment depression during Holter monitoring or exercise stress testing had similar ages (59 +/- 6 versus 58 +/- 6 years) and did not differ for tobacco smoking, plasma lipid levels, blood pressure values and prevalence of echocardiographic left ventricular hypertrophy (57% of patients had left ventricular mass indexes > or = 134 g/m2 for men and > or = 110 g/m2 for women in both groups). Women had a higher prevalence of ST-segment depression than did men during Holter monitoring [32 of 183 (17.5%) versus 11 of 213 (5.2%)], whereas the prevalences of ischemia during the exercise stress test were similar. Female sex was the only significant factor associated with the occurrence of silent myocardial ischemia [odds ratio 2.56 (95% confidence interval 1.40-4.71)]. Our results show that 15% of patients with mild-to-moderate hypertension, who are free of clinical signs of coronary artery disease, experience episodes of ST-segment depression during Holter monitoring or exercise stress testing. Most of these episodes are asymptomatic and are not associated with the severity of hypertension, the presence of left ventricular hypertrophy, and other risk factors for coronary artery disease. Episodes of ST-segment depression are more common for women than they are for men, particularly during Holter monitoring. The early detection of silent myocardial ischemia by Holter monitoring or by the exercise stress test might be useful for the identification of hypertensive patients who should be investigated further and administered a more specific treatment.

虚血性心疾患と心拍変動 日常生活における心筋虚血発症前の自律神経の変化

虚血性心疾患と心拍変動 日常生活における心筋虚血発症前の自律神経の変化

Silent ischemia after uncomplicated myocardial infarction: lack of incremental clinical significance

To determine the potential utility of the detection of silent myocardial ischemia after acute myocardial infarction for clinical decision making, we investigated the hypothesis that the occurrence of silent myocardial ischemia on ambulatory electrocardiographic (EGG) monitoring after acute myocardial infarction is independently predictive of adverse outcome in patients in whom conventional clinical and investigative parameters indicate favourable prognosis on medical therapy. Among 465 consecutive patients admitted to our Coronary Care Unit with acute myocardial infarction, 42 patients (39% of those eligible) were randomly selected for study. Twenty-four hour ambulatory ECG monitoring was carried out 13 ± 10 (standard deviation) days post-acute myocardial infarction. Ninety-eight percent of patients were receiving prophylactic anti-ischemic medications and 81% on aspirin. Silent myocardial ischemia was detected in 14%. During the follow-up period of 16 ± 3 months, acute ischemic events occurred in 33% of those with silent myocardial ischemia and 19% of those without previous silent myocardial ischemia ( P = 0.59). The sensitivity of the test for prediction of future acute ischemic events was 22% (95% confidence interval: 3–60%), specificity 87% (95% confidence interval: 72–97%), positive predictive value 33% (95% confidence interval: 4–78%) and negative predictive value 81% (95% confidence interval: 64–92%). Therefore the detection of ambulatory silent myocardial ischemia after acute myocardial infarction is not of sufficient incremental value as a predictor of the occurrence of adverse cardiac events to justify its routine clinical use in this subgroup of patients.

Heart rate variability before the occurrence of silent myocardial ischemia during ambulatory monitoring

Thirty-three ischemic episodes in 19 patients with stable coronary artery disease were studied to clarify changing autonomic nervous system activity during daily life before the occurrence of myocardial ischemia. Nonischemic points were studied for comparison of control data with ischemic episodes. These were defined as (1) patient showing no ischemic ST-T change while having the same heart rate with onset of ischemic episodes, and (2) presence within 1 to 2 hours before or after onset of ischernic episodes in the same patient. We analyzed heart rate (HR) variability during the 30-minute period before the onset and after the end of ischemic episodes during 24-hour monitoring. The period of 30 to 40 minutes before ischemia was regarded as the baseline, and HR variability was analyzed at 10-minute intervals before each ischemic episode and nonischemic point. HR variability was quantified on the band of 2 components: low frequency (0.04 to 0.15 Hz; LF) and high frequency (0.15 to 0.40 Hz; HF). Of the 33 episodes, 24 (73%) had a greater LF/HF value during the 30-minute period before ischemia than that before the nonischemic points. Distribution of the number of the 24 episodes demonstrated circadian rhythm with a peak from 8 to 10 A.M. HF power began to decrease from the last 10 minutes before ischemia, compared with baseline. A significant decrease in HF power with a background of greater value of LF/HF may explain the reduced ischemic threshold for ischemia during daily life.

Silent ischemia in unstable angina is related to an altered cardiac norepinephrine handling.

Inferential evidence suggests that silent ischemia might be related to sympathetic activity. Study of [3H]norepinephrine kinetics is a suitable tool to assess the regional sympathetic activity. This method was applied to investigate whether silent myocardial ischemia in unstable angina is related to and depends on cardiac sympathetic overactivity. Patients with active unstable angina were compared with patients with inactive unstable angina, stable effort angina, and controls. Silent myocardial ischemia was evaluated by three 24-hour Holter monitoring periods on alternate days, and [3H]norepinephrine kinetics was assessed under rest conditions and following the cold pressor test. Simultaneously, catecholamine concentrations were measured in the aortic, coronary sinus, and peripheral venous blood. Different than the other groups (p = 0.0013), in patients with active unstable angina, the majority of silent ischemic episodes occurred without increase in heart rate. These patients had a positive coronary sinus-aorta norepinephrine gradient, both at rest and following the cold pressor test. [3H]Norepinephrine kinetics demonstrated an increased selective cardiac spillover, both at rest and, even more, after the cold pressor test. Reduced cardiac [3H]norepinephrine extraction also was found. A significant relation was found between the number of ischemic episodes or the overall duration of silent ischemia and norepinephrine spillover, both at rest and following cold application. During the acute phase of unstable angina (but not in the quiescent phase or in stable effort angina), a disorder in cardiac norepinephrine handling occurs. This results in a reflex cardiac sympathetic overactivity that plays a major role in the occurrence of silent myocardial ischemia.

Effects of bisoprolol on the circadian distribution of silent myocardial ischemia and frequency domain parameters of heart rate variability

The autonomic nervous system is believed to play an important role in the occurrence of silent myocardial ischemia (SMI). To investigate the effect of bisoprolol on the circadian distribution of SMI and heart rate variability (HRV) we studied 5 patients with/> 4 episodes of SMI during 48 h Holter registration after a placebo run-in period. Patients were treated 4 weeks with bisoprolol 10 mg once daily. Spectral analysis of HRV was performed using a FFT algorithm, resulting in low frequency (LF, 0.04-0.15 Hz), high frequency components (HF, 0.15-0.40 Hz) and L F / H F ratio.

Clinical aspects of silent myocardial ischemia in China

Since the recognition of silent myocardial ischemia, there has been controversy about its prevalence among different patient subgroups. 1–4 There has also been controversy over the frequency and diagnostic applicability of asymptomatic ST-segment depression found during ambulatory electrocardiographic monitoring. 5 Also, few data exist on the occurrence of silent myocardial ischemia among different ethnic groups. This report describes the occurrence of ambulatory monitored ST-segment depression in a large group of Chinese subjects.

Current concepts of silent myocardial ischemia

The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.

Circadian patterns of myocardial ischemia

In this overview we studied evidence for the occurrence of silent myocardial ischemia, its pathophysiologic mechanisms, and the circadian distribution of ischemic episodes. The correlation between many hemodynamic parameters and their potential as drug targets was assessed. ECG evidence of myocardial ischemia (ST segment), a parameter often used in exercise tests, also occurs during ambulatory monitoring. Use of the isotope rubidium-82 and positron emission tomography helped confirm the significance of these changes in the ST segment, both painful and silent. Ischemia was detected by a reduction in the uptake of the isotope in a region of the heart reflecting a decrease in myocardial blood flow. Also it was shown that both painful and silent ischemia are caused by similar pathophysiologic mechanisms; such mechanisms include alterations in coronary blood flow and increases in myocardial oxygen demand. Episodes of ST segment depression show a circadian rhythm similar to that seen for heart rate and catecholamine release. The basic pattern shows a low incidence of ischemia at night, followed by a primary peak on rising, a decrease at midday, and then a secondary peak in the evening, with a final decrease again at night. Similar circadian rhythms have been described for acute cardiovascular events, and this may be important for treatment.