CCB (uptodate 19.3)
¾²ÀÌ´Â °÷
l stable angina pectoris if there are contraindications or adverse reactions to either beta blockers or nitrates or if symptoms are not well controlled with a combination of these agents.(BB¿¡ ¿ì¼±¼øÀ§¹Ð¸²) , ÈäÅëÁÙÀÓ
l vasospastic angina
l hypertension
l hypertrophic cardiomyopathy
l supraventricular arrhythmias
ACS¿¡¼´Â ¿Ö ¾È¾²´Â°¡?
DHP AMI ȯÀÚ¿¡¼ óÀ½¿¡´Â À̷лó periinfarct zone¿¡ necrosis¹üÀ§¸¦ ÁÙ¿©ÁÙ°ÍÀÌ¶ó °¡Á¤ÇÏ°í µµ¿òÀ» ÁÙ°ÍÀ̶ó°í »ý°¢Çϰí trial(short acting nifedipine)À» ÇßÀ¸³ª, ÇØº¸´Ï±î mortality Áõ°¡·Î ÀÌÁ¦ ¾È¾¸ ¿øÀÎ ¹Ýº¹µÈ ÀúÇ÷¾Ð°ú ±³°¨½Å°æÇ×ÁøÀ¸·Î »ý°¢µÊ
2¼¼´ë CCB (amlodipine,felodipine) : AMI ¿¡ ¿¬±¸´Â ½ÃÇàµÈ °ÍÀÌ ¾ø°í, HF, stable anginaÀÇ ¿¬±¸¿¡¼´Â À̵浵 ÇØ¾Çµµ ¾ø¾ú´Ù.
±×·¯³ª, AMIÀÇ HTNȯÀÚ¿¡¼ BP°¡ BB , ACEI or ARB·Î Á¶ÀýµÇÁö ¾ÊÀ» ¶§ ¾²°í ÀÖ´Ù.
NDHP(limited role in preventing nonfatal reinfarction) :
MDPIT trial (diltiazem À» after AMI ȯÀÚ¿¡°Ô ÁÖ°í 25°³¿ù f/u Çß´õ´Ï, »ç¸Á·ü Àç¹ß·ü Â÷ÀÌ ¾ø´õ¶ó) LV functionÁÁÀº ¼ºê±×·ì¿¡¼´Â cadiac event ÁÙ¿´´Ù. LV function¾ÈÁÁÀº ¼ºê±×·ìÀº evet,»ç¸Á·ü Áõ°¡.
INTERCEPT trial systolic HF¾ø´Â AMI onset 36-96½Ã°£¿¡ ½ÃÀÛ Diltiazem ÁÖ°í 6°³¿ùÈÄ f/u Â÷ÀÌ ¾ø´õ¶ó. ,
A pilot study : early¿¡ diltiazem IV·Î ÁÖ´Ï »ç¸Á·ü, Àç°æ»ö·ü, ÀçÇãÇ÷ÀÌ ÁÙ¾ú´Ù.
DAVIT II trial AMI 2ÁÖÈÄ¿¡ verapamil Á൵ »ç¸Á·ü, cadiac event Â÷ÀÌ ¾ø´õ¶ó. ¿ª½Ã LV function ÁÁÀº ±×·ì¿¡¼´Â »ç¸Á·ü, event°¨¼Ò, LV function ³ª»Û ±×·ì¿¡¼´Â Â÷ÀÌ ¾øÀ½
BB°¡ contraIdxÀÌ¸é¼ LV dysfunction, HF, AV block ¾øÀ»¶§¸¸ BB´ë½Å¿¡ MI¿¡ ¾µ¼ö ÀÖ´Ù.(»ç¸Á·ü event rate³·Ãã)
AF RVR, Af RVR ÀÌ¸é¼ MI¿¡, BB°¡ contraIdxÀÌ¸é¼ LV dysfunction, HF, AV block ¾øÀ»¶§¸¸ BB´ë½Å¿¡ ¾µ¼ö ÀÖ´Ù.
ACS °£´Ü¿ä¾à : amlodipine, felodipine Àº ACS¿¡¼ ¾µÀÏÀÌ ¾ø´Âµ¥, Ç÷¾ÐÀÌ Á¶Àý¾ÈµÇ¸é Ãß°¡·Î ½áº¼¼ö ÀÖ´Ù.
NDHP ACS¿¡¼ ¾µÀÏÀÌ ¾ø´Âµ¥, BB¸ø¾µ »óȲÀÌ°í ¹ÚÃâ·® ±¦ÂúÀ¸¸é ½áº¼¼ö ÀÖ°í, »ç¸Á·ü ¹× event rate¸¦ ³·Ãá´Ù.(ACS¿¡¼´Â ACEI, BB¸¦ ²À¾´´Ù. CCB¸¦ °°ÀÌ ¾µ¼ö´Â ¾ø´Ù. ¿ì¼±¼øÀ§¹Ð¸² ³»»ý°¢)
HF¿¡¼´Â
vasodilationÀ¸·Î afterload¸¦ ÁÙ¿©¼ systolic HF¿¡ È¿°ú°¡ ÀÖÀ» °ÍÀ¸·Î ±â´ëµÇ¾úÀ¸³ª, ¿¬±¸ÀÇ °á°ú negative inotrphic È¿°ú·Î ÀÓ»óÀû ¾ÇȵÊ
amlodipine, felodipine´Â HF, stable anginaÀÇ ¿¬±¸¿¡¼´Â À̵浵 ÇØ¾Çµµ ¾ø¾ú´Ù . µû¶ó¼ systolic HF°¡Áø ȯÀÚÀÇ °íÇ÷¾ÐÄ¡·á, anginaÄ¡·á¿¡ ¾ÈÀüÇÏ°Ô ¾µ ¼ö ÀÖ´Ù. ÇÏÁö¸¸, HTN¿¡¼´Â ACE, BB¸¦ ¸ÕÀú ¾²°í, angina, Afib¿¡¼´Â BB¸¦ ¸ÕÀú ½á¾ßÇÑ´Ù.
±×¿Ü DHP , NDHP ´Ù ¾È¾´´Ù.
HF°£´Ü¿ä¾à : HF¿¡¼´Â ¾È¾²´Âµ¥, amlodipine, felodipineÀº HFȯÀÚ°¡ Ç÷¾ÐÁ¶ÀýÀÌ ¾ÈµÇ¸é Ãß°¡·Î ¾µ¼ö ÀÖ°Ú´Ù(³»»ý°¢)
DHP
potent vasodilators than either verapamil or diltiazem.
vasodilate coronary arteries
blockade of calcium influx as well as an increase the levels of nitric oxide and bradykinin;
They elicit a strong reflex beta-adrenergic response,
only a mild negative inotropic effect,
NDHP
verapamil
angina : decreases myocardial oxygen demand( by negative ino, chrono, lower BP)
HF¿¡¼´Â HF¸¦ ¾ÇȽÃų¼ö ÀÖ´Ù(negative ino)
Changes in contractility are minimal in patients without heart disease
much less potent vasodilator than the dihydropyridines
Diltiazem
a potent coronary but a mild arterial vasodilator
improved blood flow through coronary epicardial vessels, collaterals
lowering mean arterial pressure
depress sinus node automaticity and AV nodal conduction time
not a negative inotrope.
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