心血管疾患と診断

Background: Many chronic conditions, as diabetes (DM) and cardiovascular Diseases suffer Major Adverse Cardiac Events (MACE): i myocarditis, congestive heart failure (CHF), Ventricular Tachycardia (VT), Ventricular Fibrillation (VF), Acute Coronary Syndromes [ACSs], and Sudden Cardiac Death (SCD) Acute infections, like COVID-19 also involve oxidative stress, leading to increased Sympathetic tone (S) and decreased Parasympathetic tone (P), increasing Sympathovagal Balance (SB) and MACE. The antioxidant (r)alpha lipoic acid (ALA) improves SB. The antianginal Ranolazine (RAN), also an antioxidant is an anti-arrhythmic. Our studies of their effects on MACE in DM, and non-DM patients with CHF, ventricular arrhythmias and SCD are reviewed herein, as our findings may apply to acute diseases, such as COVID-19.

Methods: In a case-control study, 109 CHF patients, 54 were given adjunctive off-label RAN added to ACC/AHA Guideline therapy (RANCHF). MACE and SB were compared with 55 NORANCHF patients; mean f/u 23.7 mo. 59 adults with triggered premature ventricular contractions (PVCs), bigeminy, and VT were given off-label RAN. Pre and post-RAN Holters were compared; mean f/u 3.1mo. 133 DM II with cardiac diabetic autonomic neuropathy were offered (r)ALA; 83 accepted; 50 refused. P&S were followed a mean of 6.31yrs, and SCDs recorded.

Results: (1) 70% of RANCHF patients increased LVEF 11.3 EFUs (p≤0.003), SCD reduced 56%; VT/VF therapies decreased 53%. (2) 95% of patients responded: VT decreased 91% (p<0.001). (3) SCD was reduced 43% in DM II patients taking (r)ALA (p=0.0076). Conclusions: RAN, (r) ALA treat CHF, VT, and prevent SCD. Trials in COVID-19 are needed.

Backgraund: Fractional flow reserve (FFR) measures the flow reserve of narrowed coronary arteries. It is calculated simply as the ratio of hyperemic distal coronary pressure (Pd) to aortic pressure (Pa) (Pd/Pa). We aimed to examine the relationship between arterial blood pressure normalization and FFR in hypertensive patients.

Methods: Twenty patients (14 males, 6 females; age 62.7±6.1 years) who underwent coronary angiography (CAG) with a diagnosis of stable coronary artery disease (CAD), and had 50–70% stenosis in their coronary arteries and a blood pressure higher than 140/90 mmHg in the catheter laboratory, were included in this study. The total number of lesions studied was 20. FFR was measured using a pressure measurement wire from Certus (St. Jude Medical, St. Paul, MN, USA). Measurements were made with 150 mcg adenosine in the left anterior descending (LAD) and circumflex (Cx) arteries and 100 mcg in the right coronary artery (RCA). A FFR <0.80 was considered significant in both measurements, which were repeated after blood pressure normalization with nitroglycerin infusion at 20 mcg/min. The difference between the measurements [nitrate (-), nitrate (+]) was analyzed.

Results: Of the 20 lesions evaluated, 1 was in the left main coronary artery, 9 in the LAD, 6 in the Cx, and 4 in the RCA) Systolic, diastolic and mean blood pressure decreased significantly after nitroglycerin infusion (p <0.0001). There was no significant difference between nitrate (-) and nitrate (+) in baseline FFR measurements (p <0.084). There was a significant difference between nitrate (-) and nitrate (+) patients in FFR measurements after hyperemia (p <0.005). In two patients with significant FFR measurements prior to nitrate, FFR lost its significance after a blood pressure decrease following nitrate infusion.

Conclusion: In hypertensive individuals, hyperemia-related FFR values are significantly increased after normalization of blood pressure. In the evaluation of moderate coronary lesions of hypertensive patients with FFR, decreasing the mean blood pressure to normal values may be important for preventing unnecessary interventions.

Background: Many chronic conditions, as diabetes (DM) and cardiovascular Diseases, suffer Major Adverse Cardiac Events (MACE): i myocarditis, congestive heart failure (CHF), Ventricular Tachycardia (VT), Ventricular Fibrillation (VF), Acute Coronary Syndromes [ACSs], and Sudden Cardiac Death (SCD) Acute infections, like COVID-19, also involve oxidative stress, leading to increased Sympathetic tone (S) and decreased Parasympathetic tone (P), increasing Sympathovagal Balance (SB) and MACE. The antioxidant (r) alpha lipoic acid (ALA) improves SB. The anti-anginal Ranolazine (RAN), also an antioxidant, an anti-arrhythmic. Our studies of their effects on MACE, in DM, and non-DM patients with CHF, ventricular arrhythmias and SCD are reviewed herein, as our findings may apply to acute diseases, such as COVID-19.

Methods: In a case-control study, 109 CHF patients, 54 were given adjunctive off-label RAN added to ACC/AHA Guideline therapy (RANCHF). MACE and SB were compared with 55 NORANCHF patients; mean f/u 23.7 mo. 59 adults with triggered premature ventricular contractions (PVCs), bigeminy, and VT were given off-label RAN. Pre- and post-RAN Holters were compared; mean f/u 3.1 mo. 133 DM II with cardiac diabetic autonomic neuropathy were offered (r) ALA; 83 accepted; 50 refused. P&S were followed a mean of 6.31 yrs, and SCDs recorded.

Results: (1) 70% of RANCHF patients increased LVEF 11.3 EFUs (p≤0.003), SCD reduced 56%; VT/VF therapies decreased 53%; (2) 95% of patients responded: VT decreased 91% (p<0.001); (3) SCD was reduced 43% in DM II patients taking (r) ALA (p=0.0076).

Conclusions: RAN, (r) ALA treat CHF, VT, and prevent SCD. Trials in COVID-19 are needed.

The relationship between metabolic diseases such as T2DM and regional fat deposits, particularly epicardial adipose tissue (EAT) and pericardial adipose tissue (PAT), play an important role in the development of cardiovascular diseases (CVD). Both EAT and PAT are a subset of visceral adipose tissue (VAT) associated with T2DM. They are metabolically active visceral fat deposits found around the heart, that are strongly associated with CVD including coronary artery disease (CAD) and the development of cardiac arrhythmias, predominantly due to the secretion of proinflammatory mediators and cytokines. In this paper, we review the emerging evidence of impact of T2DM on VAT and the specific role of EAT and PAT both as a cardiac risk marker and as a potentially active player in the development of cardiovascular pathology.

Globally, cardiovascular disease (CVD) is considered to be an important cause of mortality. The proper functioning of mitochondria is essential in tissues and organs which require high energy, involving the heart. Mitochondria are extremely sensitive towards nutrient and oxygen supply and experience metabolic adaptation due to the change in environment. Such adaptation is damaged in CVD that sequentially results in the degeneration of mitochondrial function correlated with irregularities in the respiratory chain and ATP production, raised oxidative stress, and loss of the structural integrity of mitochondria. Uncoupling of the respiratory chain in dysfunctional mitochondria leads to higher production of reactive oxygen species(ROS), reduction of cell ATP pool, massive cell damage, and apoptosis of cardiomyocytes. In a mitophagy process, cells clear themselves from impaired and dysfunctional mitochondria by autophagic mechanism. During heart failure, this process gets deregulated which leads to the accumulation of dysfunctional mitochondria and the situation became more adverse. Abnormalities of the respiratory chain activity and ATP synthesis may be reflected as a core of mitochondrial dysfunction in cardiac pathology. Indeed, the main objective for improvement of mitochondrial dysfunction in CVD is to therapeutically restore these vital functional properties.