We report one male patient aged 28-years undergoing total pericardiectomy for chronic calcific pericarditis with an uneventful postoperative course. The step-by-step surgical procedure of total pericardiectomy via modified left anterolateral thoracotomy without utilizing cardiopulmonary bypass has been detailed.

Coronary artery embolism is an uncommon cause of acute myocardial infarction (AMI), while antiphospholipid syndrome (APS) is one of the rare reasons due to premature AMI. Coronary angiography can diagnose coronary artery embolism, and the positive serum of aPLs may infirm APS. We report a 32 years old man with ST-elevation AMI, without any high-risk factors of coronary artery disease. Coronary thrombosis was founded in the M1 sub-coronary of Left Anterior Descending (LAD), and the coronary artery was recanalized, the artery was not obstructive, Thrombolysis in Myocardial Infarction (TIMI) grade was III. He became shortness after exercise, the echocardiography showed his left ventricular was enlarged and LVEF was decreased. High titers of an anticardiolipin antibody (aCL) IgG of 46U (positive >20.0U), and it was positive at two dosages with an interval greater than 12 weeks. But there was no evidence of any other serum markers suggesting other associated pathologies such as SLE, so the primary APS was diagnosed. We gave him anticoagulation with warfarin and a single antiplatelet with Aspirin, the target INR was 2.5-3.0. Meanwhile, statins and hydroxychloroquine (HCQ) were all prescribed. After 6-months follow-up, his heart failure symptoms were disappeared, the LVDd and LVEF were all normal, the titer was decreased to nearly normal. In clinical background, young AMI without traditional high-risk factors of CAD, we should suspect APS. Therefore, we believed that HCQ may low thrombotic rate, down-trending aPLs titer, and prevent thrombotic recurrences in patients with primary antiphospholipid syndrome.

Introduction: Mechanical revascularization of the infarct-related artery (IRA) is the most effective treatment modality in ST-segment elevation myocardial infarction (STEMI).No-reflow occurs in ~8.8-10% of cases of primary percutaneous coronary intervention(PCI) in STEMI patients. Intracoronary tenectaplase was used when there was huge thrombus causing no flow in coronary artery following primary PCI in STEMI patients. Methods: Five hundred and eighty primary PCI patients were studied over a period of two years i.e. January 2016 to December 2017. Drug eluting stents were used in all cases. Majority of our patients (>90%) came 6 hours after onset of chest pain. There were many patients where there was no flow even after mechanical thrombus aspiration and pharmacological vasodilator therapy. We have given 20 mg of tenectaplase through microcatheter in those cases. Results: There were 44 cases of no flow in our series (7.75%). TIMI 3 Flow was reestablished in thirty two patients after intracoronary tenectaplase (72%). Amongst twelve failure cases LAD involvement was most common eight cases. RCA was involved in four patients. One month mortality rate in no flow group was 50% and 6.25% in successful recanalization group. One year mortality was 12.5% in successful recanalization group and 66% in no flow group. Both were statistically significant. Conclusion: Refractory no reflow during primary PCI in STEMI is associated with high mortality and morbidity. There is no established strategy to solve this phenomenon. Intracoronary thrombolysis is an option to salvage these patients.

Background: Many chronic conditions, as Diabetes Mellitus (DM) and cardiovascular Diseases, suffer Major Adverse Cardiac Events (MACE): 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 antiarrhythmic. 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: (1) 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. (2) 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. (3) 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 years, 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). Conclusion: RAN, (r) ALA treat CHF, VT, and prevent SCD. Trials in COVID-19 are needed.

Myocardial Infarction in the absence of obstructive coronary artery disease [MINOCA] is seen in 5-6% of the patients presenting with myocardial infarction. While patients with MINOCA can present with either ST segment elevation or non-ST segment elevation myocardial infarction, they are less likely to have ST segment deviation on electrocardiography and have less of cardiac biomarker elevation compared to their obstructive coronary artery disease counterparts. Patients with MINOCA are usually younger and with lower prevalence of traditional cardiovascular risk factors compared with patients presenting with obstructive coronary artery disease. A variety of atherosclerotic and non-atherosclerotic mechanisms can lead to MINOCA. A diagnosis of MINOCA can only be made in patients whose clinical presentation is attributed to an ischemic event after excluding obstructive coronary artery disease and alternate causes for troponin elevation. A systematic approach to diagnosing the underlying causes is warranted to optimally treat patients presenting with MINOCA.