The Promise of Cilnidipine in Hypertension with Comorbidities: National Consensus Statement: National Consensus Group Comprises Cardiologists, Nephrologists, and Diabetologists from India in a National Meet at New Delhi held on 22nd May 2022.

The rapidly increasing burden of hypertension is responsible for premature deaths from cardiovascular disease (CVD), renal disease, and stroke, with a tremendous public health and financial burden. Hypertension detection, treatment, and control vary worldwide; it is still low, particularly in low- and middle-income countries (LMICs). High blood pressure (BP) and CVD risk have a strong, linear, and independent association. They contribute to alarming numbers of all-cause and CVD deaths. A major culprit for increased hypertension is sympathetic activity, and further complications of hypertension are heart failure, ischemic heart disease (IHD), stroke, and renal failure. Now, antihypertensive interventions have emerged as a global public health priority to reduce BP-related morbidity and mortality. Calcium channel blockers (CCB) are highly effective vasodilators. and the most common drugs used for managing hypertension and CVD. Cilnidipine, with both L- and N-type calcium channel blocking activity, is a promising 4th generation CCB. It causes vasodilation via L-type calcium channel blockade and inhibits the sympathetic nervous system (SNS) via N-type calcium channel blockade. Cilnidipine, which acts as a dual L/N-type CCB, is linked to a reduced occurrence of pedal edema compared to amlodipine, which solely blocks L-type calcium channels. The antihypertensive properties of cilnidipine are very substantial, with low BP variability and long-acting properties. It is beneficial for hypertensive patients to deal with morning hypertension and for patients with abnormal nocturnal BP due to exaggerated sympathetic nerve activation. Besides its BP-lowering effect, it also exhibits organ protection via sympathetic nerve inhibition and renin-angiotensin-aldosterone system inhibition; it controls heart rate and proteinuria. Reno-protective, neuroprotective, and cardioprotective effects of cilnidipine have been well-documented and demonstrated.

Role of Iron Therapy in Heart Failure: A Consensus Statement from India.

Iron deficiency (ID) with or without anemia is frequently observed in patients with heart failure (HF). Uncorrected ID is associated with higher hospitalization and mortality in patients with acute HF (AHF) and chronic HF (CHF). Hence, in addition to chronic renal insufficiency, anemia, and diabetes, ID appears as a novel comorbidity and a treatment target of CHF. Intravenous (IV) ferric carboxymaltose (FCM) reduces the hospitalization risk due to HF worsening and improves functional capacity and quality of life (QOL) in HF patients. The current consensus document provides criteria, an expert opinion on the diagnosis of ID in HF, patient profiles for IV FCM, and correct administration and monitoring of such patients.

Angiotensin Receptor-Neprilysin Inhibitor Therapy and Cardiac Remodeling in Heart Failure: Consensus Statement from India.

Adverse cardiac remodeling refers to progressive structural and functional modifications in the heart because of increased wall stress in the myocardium, loss of viable myocardium, and neurohormonal stimulation. The guideline-directed medical therapy for Heart failure (HF) includes Angiotensin receptor-neprilysin inhibitor (ARNI) (sacubitril/valsartan), ß-blockers, sodium-glucose co-transporter 2 (SGLT2) inhibitors, and mineralocorticoid receptor antagonists (MRA). ARNI is under-prescribed in India despite its attractive safety and efficacy profile. Therefore, the consensus discusses objectives and topics related to ARNI in the management of cardiac remodeling, and experts shared their views on the early timely intervention of effective dosage of ARNI to improve the diagnosis and enhance mortality and morbidity benefits in cardiac reverse remodeling (CRR).

Diagnosis of a thrombosed bileaflet prosthetic mitral valve by real-time three-dimensional transesophageal echocardiography.

Mitral valve replacement, hence thrombosis of prosthetic heart valves (PHV) are not uncommon in our country. The diagnosis is commonly established by increased gradients across PHV during transthoracic echo and restricted leaflet movement during transesophageal echo or fluoroscopy. We demonstrated the leaflets of a bileaflet PHV, of which one was stuck in closed position and the movement of the other was partially restricted by real-time three-dimensional transesophageal echocardiography.

The mitral valve: characterisation by real-time three-dimensional transesophageal echocardiography. Current status.

The complex anatomy of mitral valve demands precise and sophisticated imaging during any intervention .Transesophageal echocardiography has been the most frequently used modality. With the advent of three-dimensional echocardiography a more comprehensive description of the mitral valve is now possible. This review aims to discuss the framework for imaging the mitral valve by three-dimensional echocardiography; its current status and the limitations of three-dimensional echocardiography in its current platform.

Thrombotic occlusion of bilateral popliteal arteries by ball valve thrombus in left atrium.

We present a patient of mitral stenosis with a left atrial ball valve thrombus. The diagnosis was confirmed by transesophageal echocardiogram. No clot was detected in the left atrium or the left atrial appendage at surgery. At completion of surgery, the distal pulses of lower limbs were not palpable. Vascular Doppler study of lower limbs revealed thrombus-laden bilateral popliteal arteries. Emergency vascular surgery restored circulation in lower limb vessels.

Protein C deficiency leading to pulmonary thromboembolism in a patient with hereditary spherocytosis.

Hereditary protein C deficiency results in a hypercoagulable state that can manifest itself as venous thrombosis and pulmonary embolism. The prevalence of this condition, even among patients with familial thrombosis, is quite low. We report a case of protein C deficiency presenting as massive pulmonary thromboembolism in a patient with hereditary spherocytosis, an uncommon hemolytic disorder not usually associated with increased thrombotic risk. A review of the literature revealed only a few cases of thrombosis associated with hereditary spherocytosis, and none of them had protein C deficiency. This makes the present case the first of its kind to be reported.